Difference between revisions of "Virus"

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{{Taxobox
{{otheruses1|biological infectious particles}}
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| color = violet
 
 
{{Taxobox | color=violet
 
 
| name = Viruses
 
| name = Viruses
| image = Herpes_simpex_virus.jpg
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| image = Rotavirus Reconstruction.jpg
| image_caption = Herpes simplex virus 1 (HSV-1)
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| image_caption = Rotavirus
 
| virus_group = I–VII
 
| virus_group = I–VII
 
| subdivision_ranks = Groups
 
| subdivision_ranks = Groups
| subdivision = I: [[dsDNA virus]]es<br>
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| subdivision =
II: [[ssDNA virus]]es<br>
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I: [[dsDNA virus]]es<br />
III: [[dsRNA virus]]es<br>
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II: [[ssDNA virus]]es<br />
IV: [[positive-sense ssRNA virus|(+)ssRNA virus]]es<br>
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III: [[dsRNA virus]]es<br />
V: [[negative-sense ssRNA virus|(-)ssRNA virus]]es<br>
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IV: [[positive-sense ssRNA virus|(+)ssRNA virus]]es<br />
VI: [[ssRNA-RT virus]]es<br>
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V: [[negative-sense ssRNA virus|(-)ssRNA virus]]es<br />
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VI: [[ssRNA-RT virus]]es<br />
 
VII: [[dsDNA-RT virus]]es
 
VII: [[dsDNA-RT virus]]es
 
}}
 
}}
A '''virus''' (from the [[Latin]] noun ''virus'', meaning [[toxin]] or [[poison]]) is a sub-[[microscopic]] particle (ranging in size from about 15–600 [[Nano|n]][[Metre|m]]) that can [[infectious diseases|infect]] the [[cell (biology)|cell]]s of a [[biological]] [[organism]]. Viruses can replicate themselves only by infecting a host cell. They therefore cannot reproduce on their own. At the most basic level, viruses consist of [[genetic material]] contained within a protective [[protein]] coat called a [[capsid]]. They infect a wide variety of organisms: both [[eukaryote]]s (animals, plants, [[protist]]s, and [[fungi]]) and [[prokaryote]]s ([[bacteria]] and [[archaea]]). A virus that infects bacteria is known as a ''[[bacteriophage]]'', often shortened to ''phage''. The study of viruses is known as [[virology]] and people who study viruses are known as virologists. Viruses cause several serious human diseases, such as [[AIDS]], [[influenza]] and [[rabies]]. Therapy is difficult for viral diseases as [[antibiotic]]s have no effect on viruses and few [[antiviral drug]]s are known. The best way to prevent viral diseases is with a [[vaccine]], which produces [[immunity (medical)|immunity]].
 
  
It has been argued extensively whether viruses are living organisms. Most virologists consider them non-living,<ref>[http://school.discovery.com/lessonplans/programs/understandingviruses/ http://school.discovery.com/lessonplans/programs/understandingviruses/]</ref><ref>[http://www.tulane.edu/~dmsander/garryfavwebfaq.html http://www.tulane.edu/~dmsander/garryfavwebfaq.html]</ref><ref>[http://library.thinkquest.org/CR0212089/virus.htm http://library.thinkquest.org/CR0212089/virus.htm]</ref> as they do not meet all the criteria of the generally accepted definition of [[life]]. For example, unlike living organisms as defined, viruses do not respond to changes in the environment nor do they consist of [[Cell (biology)|cells]], generally regarded as the fundamental unit of life.
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__NOTOC__
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A '''virus''' (from the Latin ''virus'' meaning "toxin" or "poison"), is a [[Optical microscope#Limitations of light microscopes|sub-microscopic]] infectious agent that is unable to grow or reproduce outside a [[host (biology)|host]] [[cell (biology)|cell]]. Each viral particle, or '''virion''', consists of genetic material, [[DNA]] or [[RNA]], within a protective protein coat called a [[capsid]]. The capsid shape varies from simple helical and icosahedral (polyhedral or near-spherical) forms, to more complex structures with tails or an [[viral envelope|envelope]]. Viruses infect cellular life forms and are grouped into animal, plant and bacterial types, according to the type of host infected.
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Biologists debate whether or not viruses are living organisms. Some consider them non-living as they do not meet the criteria of the definition of [[life]]. For example, unlike most organisms, viruses do not have [[Cell (biology)|cells]]. However, viruses have genes and evolve by [[natural selection]]. Others have described them as organisms at the edge of life. Viral infections in human and animal hosts usually result in an immune response and [[disease]]. Often, a virus is completely eliminated by the [[immune system]]. [[Antibiotic]]s have no effect on viruses, but [[antiviral drug]]s have been developed to treat life-threatening infections. [[Vaccine]]s that produce lifelong [[immunity (medical)|immunity]] can prevent viral infections.
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== Etymology ==
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The word is from the Latin ''virus'' referring to [[poison]] and other noxious substances, first used in English in 1392.<ref name=Etymology_Dictionary>{{cite web
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|title = virus
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|work = The Online Etymology Dictionary
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|url = http://www.etymonline.com/index.php?term=virus
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|accessdate = 2007-07-16
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}}</ref> ''Virulent'', from Latin ''virulentus'', "poisonous", dates to 1400.<ref name=OED>{{cite web
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|title = virulent, a.
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|work = The Oxford English Dictionary - Online
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|url = http://dictionary.oed.com
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|accessdate = 2007-07-16
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}}</ref> A meaning of "agent that causes infectious disease" is first recorded in 1728,<ref name=Etymology_Dictionary/> before the discovery of viruses by the Russian-Ukrainian [[biologist]] [[Dmitry Ivanovsky]] in 1892. The adjective ''viral'' dates to 1948.<ref name=OED2>{{cite web
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|title = viral, a.
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|work = The Oxford English Dictionary - Online
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|url = http://dictionary.oed.com
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|accessdate = 2007-07-16
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}}</ref> Today, ''virus'' is used to describe the biological viruses discussed above and as a metaphor for other parasitically-reproducing things, such as [[meme]]s or computer viruses (since 1972).<ref name=OED/> The term ''virion'' is also used to refer to a single infective viral particle. The English plural form of ''virus'' is ''viruses''.
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==Discovery of viruses==
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Viral diseases such as [[rabies]], [[yellow fever]] and [[smallpox]] have affected humans for centuries. There is hieroglyphical evidence of [[polio]] in [[ancient Egyptian medicine]],<ref>Paul GF. (1971) A History of Poliomyelitis. Yale University Press:
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New Haven and London.</ref> though the cause of this disease was unknown at the time. In the 10th century, [[Muhammad ibn Zakarīya Rāzi]] (Rhazes) wrote the ''Treatise on Smallpox and Measles'', in which he gave the first clear descriptions of smallpox and [[measles]].<ref>Abdul Nasser Kaadan (2007), [http://muslimheritage.com/topics/default.cfm?ArticleID=682 Al-Razi on Smallpox and Measles], FSTC</ref> In the 1020s, [[Avicenna]] wrote ''[[The Canon of Medicine]]'', in which he discovered the contagious nature of [[infectious disease]]s, such as [[tuberculosis]] and [[sexually transmitted disease]]s, and their distribution through bodily contact or through [[water]] and soil;<ref name=Sarton>[[George Sarton]], ''Introduction to the History of Science''.<br />([[cf.]] Dr. A. Zahoor and Dr. Z. Haq (1997), [http://www.cyberistan.org/islamic/Introl1.html Quotations From Famous Historians of Science], Cyberistan.</ref> stated that bodily [[secretion]] is contaminated by "foul foreign earthly bodies" before being infected;<ref name=Syed/> and introduced the method of [[quarantine]] as a means of limiting the spread of contagious disease.<ref name=Tschanz>David W. Tschanz, MSPH, PhD (August 2003). "Arab Roots of European Medicine", ''Heart Views'' '''4''' (2).</ref>
  
==Discovery==
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When the [[Black Death]] [[bubonic plague]] reached al-Andalus in the 14th century, [[Islamic medicine#Bacteriology, epidemiology, microbiology|Ibn Khatima]] discovered that infectious diseases are caused by [[microorganism]]s which enter the human body. The etiologic cause of the bubonic plague would later be identified as a bacterium. Another 14th century Andalusian physician, [[Islamic medicine#Bacteriology, epidemiology, microbiology|Ibn al-Khatib]] (1313-1374), wrote a treatise called ''On the Plague'', in which he stated how infectious diseases can be transmitted through bodily contact and "through garments, vessels and earrings."<ref name=Syed>Ibrahim B. Syed, Ph.D. (2002). "Islamic Medicine: 1000 years ahead of its times", ''[[The Islamic Medical Association of North America|Journal of the Islamic Medical Association]]'' '''2''', p. 2-9.</ref> In 1717, Mary Montagu, the wife of an English ambassador to the Ottoman Empire, observed local women [[inoculation|inoculating]] their children against [[smallpox]].<ref name=Behbehani_1983>{{cite journal
[[Image:viren22.jpg|thumb|right|200px|Computer-generated image of virions]]
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|author=Behbehani AM
Viral diseases such as [[rabies]], [[yellow fever]] and [[smallpox]] have affected humans for many centuries. There is hieroglyphical evidence of [[polio]] in the ancient Egyptian empire,<ref name=Lewis_2000>{{cite journal | author = Lewis R | title = Polio Eradication Goal Extended | journal = The Scientist | year = 2000 | volume = 14 | issue = 24 | pages = 12 | url= http://www.the-scientist.com/article/display/12168/}}</ref> though the cause of these diseases was unknown at the time. In 1717, [[Lady Mary Wortley Montagu|Mary Montagu]], the wife of an English ambassador to the [[Ottoman Empire]], observed local women [[inoculation|inoculating]] their children against [[smallpox]].<ref name=Behbehani_1983>{{cite journal |author=Behbehani AM |title=The smallpox story: life and death of an old disease |journal=Microbiol Rev |volume=47 |issue=4 |pages=455-509 |year=1983 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=6319980 |pmid=6319980}}</ref> In the late 18th century, [[Edward Jenner]] observed and studied Miss Sarah Nelmes, a milkmaid who had previously caught [[cowpox]] and was subsequently found to be immune to [[smallpox]], a similar, but devastating virus. Jenner developed the first [[vaccine]] based on these findings; after lengthy (but successful) [[vaccination]] campaigns the [[World Health Organization]] (WHO) certified the eradication of [[smallpox]] in 1979.<ref name=WHO_Meeting_Agenda>{{cite web | title=Smallpox eradication: destruction of variola virus stocks | work= WHO: 52nd World Health Assembly | url=http://ftp.who.int/gb/pdf_files/WHA52/ew5.pdf | accessdate=2006-09-23}}</ref>
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|title=The smallpox story: life and death of an old disease
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|journal=Microbiol Rev
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|volume=47
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|issue=4
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|pages=455-509
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|year=1983
 +
|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=6319980
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|pmid=6319980
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}}</ref> In the late 18th century, [[Edward Jenner]] observed and studied Miss Sarah Nelmes, a milkmaid who had previously caught [[cowpox]] and was found to be immune to [[smallpox]], a similar, but devastating virus. Jenner developed the smallpox [[vaccine]] based on these findings. After lengthy [[vaccination]] campaigns, the [[World Health Organization]] (WHO) certified the eradication of [[smallpox]] in 1979.
  
In the late 19th century [[Charles Chamberland]] developed a porcelain filter with pores small enough to filter bacteria, yet retain all viable viruses.<ref name=Horzinek_1997>{{cite journal | author = Horzinek MC| title = The birth of virology | journal = Antonie van Leeuwenhoek | year = 1997 | volume = 71 | pages = 15&ndash;20 | doi=10.1023/A:1000197505492 }}</ref> [[Dimitri Ivanovski]] used this filter to study [[tobacco mosaic virus]]. He published experiments showing that crushed leaf extracts of infected tobacco plants were still infectious after filtering through such filters. At about the same time, several others documented filterable disease-causing agents, with several independent experiments showing that viruses were different from bacteria, yet they could also cause disease in living organisms. These experiments showed that viruses are orders of magnitudes smaller than bacteria. The term ''virus'' was coined by the Dutch microbiologist [[Martinus Beijerinck]].
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In the late 19th century, [[Charles Chamberland]] developed a porcelain filter with pores small enough to remove cultured bacteria from their culture medium.<ref name=Horzinek_1997>{{cite journal
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|author = Horzinek MC
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|title = The birth of virology
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|journal = Antonie van Leeuwenhoek
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|year = 1997
 +
|volume = 71
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|pages = 15&ndash;20
 +
|doi=10.1023/A:1000197505492
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}}</ref> [[Dimitri Ivanovski]] used this filter to study an infection of tobacco plants, now known as [[tobacco mosaic virus]]. He passed crushed leaf extracts of infected tobacco plants through the filter, then used the filtered extracts to infect other plants, thereby proving that the infectious agent was not a bacterium. Similar experiments were performed by several other researchers, with similar results. These experiments showed that viruses are orders of magnitude smaller than bacteria. The term ''virus'' was coined by the Dutch microbiologist [[Martinus Beijerinck]], who showed, using methods based on the work of Ivanovski, that tobacco mosaic disease is caused by something smaller than a bacterium. He coined the Latin phrase "contagium vivum fluidum" (which means "soluble living germ") as the first idea of the virus.<ref>Chung, King-Thom and Ferris, Deam Hunter (1996). Martinus Willem Beijerinck (1851-1931): pioneer of general microbiology. AMS News 62, 539-543. http://www.asm.org/ASM/files/CCLIBRARYFILES/FILENAME/0000000251/621096p539.pdf PDF]</ref> The first human virus identified was [[Yellow Fever]] virus.
  
In the early 20th century, [[Frederick Twort]] discovered that bacteria could be attacked by viruses. [[Felix d'Herelle]], working independently, showed that a preparation of viruses caused areas of cellular death on thin [[cell culture]]s spread on [[agar]]. Counting the dead areas allowed him to estimate the original number of viruses in the suspension. The invention of [[Electron microscopy]] provided the first look at viruses. In 1935 [[Wendell Stanley]] crystallised the tobacco mosaic virus and found it to be mostly [[protein]]. A short time later the virus was separated into protein and [[nucleic acid]] parts.  In 1939, [[Max Delbrück]] and [[E.L. Ellis]] demonstrated that, in contrast to cellular organisms, bacteriophage reproduce in "one step", rather than exponentially.
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In the early 20th century, [[Frederick Twort]] discovered that bacteria could be infected by viruses.<ref> href="http://encyclopedia.jrank.org/Cambridge/entries/067/Frederick-William-Twort.html">Frederick William Twort</ref> [[Felix d'Herelle]], working independently, showed that a preparation of viruses caused areas of cellular death on thin [[cell culture]]s spread on [[agar]]. Counting the dead areas allowed him to estimate the original number of viruses in the suspension. The invention of [[electron microscopy]] provided the first look at viruses. In 1935, [[Wendell Stanley]] crystallized the tobacco mosaic virus and found it to be mostly [[protein]].<ref name="pmid17756690">{{cite journal
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|author=Stanley WM, Loring HS
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|title=THE ISOLATION OF CRYSTALLINE TOBACCO MOSAIC VIRUS PROTEIN FROM DISEASED TOMATO PLANTS
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|journal=
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|volume=83
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|issue=2143
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|pages=85
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|year=1936
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|pmid=17756690
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|doi=10.1126/science.83.2143.85
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}}</ref> A short time later, the virus was separated into protein and [[nucleic acid]] parts.<ref name="pmid17788438">{{cite journal
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|author=Stanley WM, Lauffer MA
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|title=DISINTEGRATION OF TOBACCO MOSAIC VIRUS IN UREA SOLUTIONS
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|journal=
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|volume=89
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|issue=2311
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|pages=345–347
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|year=1939
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|pmid=17788438
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|doi=10.1126/science.89.2311.345
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}}</ref><ref name="pmid16590772">{{cite journal
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|author=Tsugita A, Gish DT, Young J, Fraenkel-Conrat H, Knight CA, Stanley WM
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|title=THE COMPLETE AMINO ACID SEQUENCE OF THE PROTEIN OF TOBACCO MOSAIC VIRUS
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|journal=Proc. Natl. Acad. Sci. U.S.A.
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|volume=46
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|issue=11
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|pages=1463–9
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|year=1960
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  |pmid=16590772
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}}</ref> In 1939, [[Max Delbrück]] and E.L. Ellis demonstrated that, in contrast to cellular organisms, bacteriophage reproduce in "one step", rather than exponentially.<ref name="pmid16791793">{{cite journal
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|author=Pennazio S
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|title=The origin of phage virology
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|journal=Riv. Biol.
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|volume=99
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|issue=1
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|pages=103–29
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|year=2006
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|pmid=16791793
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}}</ref>
  
A major problem for early virologists was the inability to propagate viruses on sterile culture media, as is done with cellular microorganisms. This limitation required medical virologists to infect living animals with infectious material, which is dangerous. The first breakthrough came in 1931, when [[Ernest William Goodpasture]] demonstrated the growth of [[influenza]] and several other viruses in fertile chicken eggs.  However, many viruses would not grow in chicken eggs, and a more flexible technique was needed for propagation of viruses. The solution came in 1949 when [[John Franklin Enders]], [[Thomas H. Weller]] and [[Frederick Chapman Robbins]] together developed a technique to grow [[polio virus]] in cultures of living animal cells.  Their methods have since been extended and applied to the growth of many viruses and other infectious agents that do not grow on sterile culture media.
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A major problem for early virologists was the inability to propagate viruses on sterile culture media, as is done with cellular microorganisms. This limitation required medical virologists to infect living animals with infectious material, which is dangerous. The first breakthrough came in 1931, when [[Ernest William Goodpasture]] demonstrated the growth of [[influenza]] and several other viruses in fertile chicken eggs.<ref name="pmid17810781">{{cite journal
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|author=Goodpasture EW, Woodruff AM, Buddingh GJ
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  |title=THE CULTIVATION OF VACCINE AND OTHER VIRUSES IN THE CHORIOALLANTOIC MEMBRANE OF CHICK EMBRYOS
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|journal=
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|volume=74
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|issue=1919
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|pages=371–372
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|year=1931
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|pmid=17810781
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|doi=10.1126/science.74.1919.371
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}}</ref> However, some viruses would not grow in chicken eggs, and a more flexible technique was needed for propagation of viruses. The solution came in 1949 when [[John Franklin Enders]], [[Thomas H. Weller]] and [[Frederick Chapman Robbins]] together developed a technique to grow the [[polio virus]] in cultures of living animal cells.<ref name="pmid15470207">{{cite journal
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|author=Rosen FS
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|title=Isolation of poliovirus--John Enders and the Nobel Prize
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  |journal=N. Engl. J. Med.
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|volume=351
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|issue=15
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|pages=1481–3
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|year=2004
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|pmid=15470207
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|doi=10.1056/NEJMp048202
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}}</ref> Their methods have since been extended and applied to the growth of viruses and other infectious agents that do not grow on sterile culture media.
  
 
==Origins==
 
==Origins==
The origins of modern viruses are not entirely clear. It may be that no single mechanism can account for all viruses. They do not [[fossil]]ize well, so [[Molecular biology|molecular techniques]] have been the most useful means of hypothesising how they arose. Research in [[microfossil]] identification and molecular biology may yet discern fossil evidence dating to the [[Archean]] or [[Proterozoic]] [[eon (geology)|eons]]. Two main hypotheses currently exist.<ref name="prescott">{{cite book | title=Microbiology| last=Prescott| first=L| date=1993| publisher=Wm. C. Brown Publishers| id=0-697-01372-3}}</ref>  
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The origin of modern viruses is not entirely clear. It may be that no single mechanism can account for their origin.<ref>Holmes EC, Drummond AJ. The evolutionary genetics of viral emergence.Curr Top Microbiol Immunol. 2007;315:51-66.</ref> They do not [[fossil]]ize well, so [[Molecular biology|molecular techniques]] have been the most useful means of hypothesising how they arose.<ref>Liu Y, Nickle DC, Shriner D, Jensen MA, Learn GH Jr, Mittler JE, Mullins JI. Molecular clock-like evolution of human immunodeficiency virus type 1.Virology. 2004 Nov 10;329(1):101-8.</ref> Research in microfossil identification and molecular biology may yet discern fossil evidence dating to the Archean or Proterozoic [[eon (geology)|eons]]. Two main hypotheses currently exist.<ref name="prescott">{{cite book
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|title=Microbiology
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|last=Prescott
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|first=L
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|date=1993
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|publisher=Wm. C. Brown Publishers
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|id=0-697-01372-3
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}}</ref>
  
Small viruses with only a few genes may be runaway stretches of nucleic acid originating from the genome of a living organism. Their genetic material could have been derived from transferable genetic elements such as [[plasmid]]s or [[transposon]]s, which are prone to moving within, leaving, and entering genomes.
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Small viruses with only a few genes may be runaway stretches of nucleic acid originating from the genome of a living organism. Their genetic material could have been derived from transferable genetic elements such as [[plasmid]]s or [[transposon]]s, that are prone to moving within, leaving, and entering genomes. New viruses are emerging ''[[de novo]]'' and therefore, it is not always the case that viruses have "ancestors".<ref>Keese P, Gibbs A. Plant viruses: master explorers of evolutionary space.Curr Opin Genet Dev. 1993 Dec;3(6):873-7.</ref>
  
Viruses with larger genomes, such as [[poxvirus]]es, may have once been small cells which parasitised larger host cells. Over time, genes not required by their parasitic lifestyle would have been lost in a streamlining process known as ''retrograde-evolution'' or ''reverse-evolution''. The bacteria [[Rickettsia]] and [[Chlamydia]] are living cells that, like viruses, can only reproduce inside host cells. They lend credence to the streamlining hypothesis, as their parasitic lifestyle is likely to have caused the loss of genes that enabled them to survive outside a host cell.
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Viruses with larger genomes, such as [[poxvirus]]es, may have once been small cells that parasitized larger host cells. Over time, genes not required by their parasitic lifestyle would have been lost in a streamlining process known as "retrograde-evolution" or "reverse-evolution". The bacteria ''[[Rickettsia]]'' and ''[[Chlamydia (bacterium)|Chlamydia]]'' are living cells that, like viruses, can only reproduce inside host cells. They lend credence to the streamlining hypothesis, as their parasitic lifestyle is likely to have caused the loss of genes that enabled them to survive outside a host cell.
  
It is hypothetically possible that viruses represent a primitive form of self replicating DNA and are a precursor to life as it is presently defined.
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It is possible that viruses represent a primitive form of self replicating DNA and are a precursor to life as it is currently defined.<ref>Koonin EV. The Biological Big Bang model for the major transitions in evolution.Biol Direct. 2007 Aug 20;2:21.</ref> Other infectious particles which are even simpler in structure than viruses include [[viroid]]s, [[satellite (biology)|satellites]], and [[prion]]s.
  
Other infectious particles which are even simpler in structure than viruses include [[viroid]]s, [[satellite (biology)|satellite]]s, and [[prion]]s.
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==Classification==
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{{main|Virus classification}}
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In [[taxonomy]], the classification of viruses is difficult owing to the lack of a fossil record and the dispute over whether they are living or non-living.<ref> Rybicki EP (1990) The classification of organisms at the edge of life, or problems with virus systematics. S Aft J Sci 86:182-186</ref><ref name="pmid13481308">{{cite journal
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|author=LWOFF A
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|title=The concept of virus
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|journal=J. Gen. Microbiol.
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|volume=17
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|issue=2
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|pages=239–53
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|year=1957
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|pmid=13481308
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|doi=}}</ref> They do not fit easily into any of the [[domain (biology)|domains]] of [[biological classification]], and classification begins at the [[family (biology)|family]] rank. However, the domain name of [[Acytota]] (without cells) has been suggested. This would place viruses on a par with the other domains of [[Eubacteria]], [[Archaea]], and [[Eukarya]]. Not all families are currently classified into orders, nor all genera classified into families.
  
==Classification==
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In 1962, [[André Lwoff]], Robert Horne, and [[Paul Tournier]] were the first to develop a means of virus classification, based on the [[Linnaean taxonomy|Linnaean]] hierarchical system.<ref name="pmid14467544">{{cite journal
{{details|Virus classification}}
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|author=LWOFF A, HORNE RW, TOURNIER P
{| class = "prettytable" style = "float:right; font-size:85%; margin-left:15px"
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|title=[[A virus system.]] |language=French
|+ Baltimore classification
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|journal=C. R. Hebd. Seances Acad. Sci.
! Group || Contains
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|volume=254
|-
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|issue=
| I || [[dsDNA virus]]es
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|pages=4225–7
|-
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|year=1962
| II || [[ssDNA virus]]es
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|pmid=14467544
|-
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|doi=}}</ref> This system based classification on [[phylum]], [[class (biology)|class]], [[order (biology)|order]], [[family (biology)|family]], [[genus]], and [[species]]. Viruses were grouped according to their shared properties (not of their hosts) and the type of nucleic acid forming their genomes.<ref name="pmid13931895">{{cite journal
| III || [[dsRNA virus]]es
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|author=LWOFF A, HORNE R, TOURNIER P
|-
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|title=A system of viruses
| IV || [[positive-sense ssRNA virus|(+)ssRNA virus]]es
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|journal=Cold Spring Harb. Symp. Quant. Biol.
|-
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|volume=27
| V || [[negative-sense ssRNA virus|(-)ssRNA virus]]es
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|issue=
|-
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|pages=51–5
| VI || [[ssRNA-RT virus]]es
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|year=1962
|-
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|pmid=13931895
| VII || [[dsDNA-RT virus]]es
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|doi=}}</ref> Following this initial system, a few modifications were made and the [[International Committee on Taxonomy of Viruses]] was developed (ICTV).
|-
 
| colspan="2" | <small>''ss: single-stranded, ds: double stranded<br>RT: reverse transcribing''</small>
 
|}
 
In [[taxonomy]], the classification of viruses is rather difficult due to the lack of a fossil record and the dispute over whether they are living or non-living. They do not fit easily into any of the [[domain (biology)|domains]] of [[biological classification]] and therefore classification begins at the [[family (biology)|family]] rank. However, the domain name of [[Acytota]] (without cells) has been suggested. This would place viruses on a par with the other domains of [[Eubacteria]], [[Archaea]], and [[Eukarya]]. Not all families are currently classified into orders, nor all genera classified into families.
 
  
As an example of viral classification, the [[chicken pox]] virus belongs to family ''[[Herpesviridae]]'', subfamily ''[[Alphaherpesvirinae]]'' and genus ''[[Varicellovirus]]''. It remains unranked in terms of order. The general structure is as follows.
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====ICTV classification====
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The [[International Committee on Taxonomy of Viruses]] (ICTV) developed the current classification system and put in place guidelines that put a greater weighting on certain virus properties to maintain family uniformity. A universal system for classifying viruses, and a unified taxonomy, has been established since 1966. In determining order, taxonomists should consider the type of nucleic acid present, whether the nucleic acid is single- or double-stranded, and the presence or absence of an [[Envelope (biology)|envelope]]. After these three main properties, other characteristics can be considered: the type of host, the capsid shape, immunological properties and the type of disease it causes. The system makes use of a series of ranked [[taxon]]s.
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The general structure is as follows:
  
 
:[[Order (biology)|Order]] (''-virales'')
 
:[[Order (biology)|Order]] (''-virales'')
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:::::[[Species]] (''-virus'')
 
:::::[[Species]] (''-virus'')
  
The [[International Committee on Taxonomy of Viruses]] (ICTV) developed the current classification system and put in place guidelines that put a greater weighting on certain virus properties in order to maintain family uniformity. In determining order, taxonomists should consider the type of nucleic acid present, whether the nucleic acid is single- or double-stranded, and the presence or absence of an [[Envelope (biology)|envelope]]. After these three main properties, other characteristics can be considered: the type of host, the capsid shape, immunological properties and the type of disease it causes.
+
The recognition of orders is very recent; to date, only three have been named, and most families remain unplaced. The committee does not formally distinguish between subspecies, strains, and isolates. In total there are three orders, 56 families, nine subfamilies, and 233 genera. ICTV recognizes about 1,550 virus species, but about 30,000 virus strains and isolates are being tracked by virologists.<ref> Virus Taxonomy 8th Reports of the International Committee on Taxonomy of Viruses C.M. Fauquet, M.A. Mayo, J. Maniloff, U. Desselberger, and L.A. Ball (eds)
 +
Academic Press, 1162 pp. (2005) Elsevier Publication Date: 27 May 2005 </ref>
 +
 
 +
The [[Nobel Prize]]-winning biologist [[David Baltimore]] devised the [[Virus classification#Baltimore classification|Baltimore classification]] system.<ref name="pmid4377923">{{cite journal
 +
|author=Baltimore D
 +
|title=The strategy of RNA viruses
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|journal=Harvey Lect.
 +
|volume=70 Series
 +
|issue=
 +
|pages=57–74
 +
|year=1974
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|pmid=4377923
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|doi=}}</ref><ref name="pmid4348509">{{cite journal
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|author=Temin HM, Baltimore D
 +
|title=RNA-directed DNA synthesis and RNA tumor viruses
 +
|journal=Adv. Virus Res.
 +
|volume=17
 +
|issue=
 +
|pages=129–86
 +
|year=1972
 +
|pmid=4348509
 +
|doi=}}</ref> The ICTV classification system is used in conjunction with the Baltimore classification system in modern virus classification.<ref name="pmid15078590">{{cite journal
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|author=van Regenmortel MH, Mahy BW
 +
|title=Emerging issues in virus taxonomy
 +
|journal=Emerging Infect. Dis.
 +
|volume=10
 +
|issue=1
 +
|pages=8–13
 +
|year=2004
 +
|pmid=15078590
 +
|doi=}}</ref><ref name="pmid10486120">{{cite journal
 +
|author=Mayo MA
 +
|title=Developments in plant virus taxonomy since the publication of the 6th ICTV Report. International Committee on Taxonomy of Viruses
 +
|journal=Arch. Virol.
 +
|volume=144
 +
|issue=8
 +
|pages=1659–66
 +
|year=1999
 +
|pmid=10486120
 +
|doi=}}</ref><ref name="pmid15183049">{{cite journal
 +
|author=de Villiers EM, Fauquet C, Broker TR, Bernard HU, zur Hausen H
 +
|title=Classification of papillomaviruses
 +
|journal=Virology
 +
|volume=324
 +
|issue=1
 +
|pages=17–27
 +
|year=2004
 +
|pmid=15183049
 +
|doi=10.1016/j.virol.2004.03.033}}</ref>
 +
 
 +
====Baltimore Classification====
 +
[[Image:Baltimore Classification.png|right|thumb|300px|The Baltimore Classification of viruses is based on the method of viral [[mRNA]] synthesis.]]
 +
{{Main|Baltimore classification}}
 +
The Baltimore classification of viruses is based on the mechanism of [[mRNA]] production. Viruses must generate positive strand mRNAs from their genomes to produce proteins and replicate themselves, but different mechanisms are used to achieve this in each virus family. This classification places viruses into seven groups:
  
In addition to this classification system, the [[Nobel Prize]]-winning biologist [[David Baltimore]] devised the [[Virus classification#Baltimore classification|Baltimore classification]] system. This places a virus into one of seven ''Groups'', which distinguish viruses based on their mode of replication and genome type. The ICTV classification system is used in conjunction with the Baltimore classification system in modern virus classification.
+
{{Baltimore groups}}
 +
 
 +
As an example of viral classification, the [[chicken pox]] virus, ''[[Varicella zoster]]'' (VZV), belongs to family [[Herpesviridae]], subfamily [[Alphaherpesvirinae]] and genus ''[[Varicellovirus]]''. It remains unranked in terms of order. VZV is in Group I of the Baltimore Classification because it is a dsDNA virus that does not use [[reverse transcriptase]].
  
 
== Structure ==
 
== Structure ==
A complete virus particle, known as a '''virion''', is little more than a [[gene]] transporter, consisting in its simplest form of [[nucleic acid]] surrounded by a protective coat of [[protein]] called a [[capsid]]. A capsid is composed of proteins encoded by the viral [[genome]] and its shape serves as the basis for [[morphology (biology)|morphological]] distinction. Virally coded protein subunits - sometimes called '''protomers''' - will self-assemble to form the capsid, generally requiring the presence of the virus genome - however, many complex viruses code for proteins which assist in the construction of their capsid.<ref name=prescott> </ref> Proteins associated with nucleic acid are known as [[nucleoprotein]]s, and the association of viral capsid proteins with viral nucleic acid is called a '''nucleocapsid'''.
+
A complete virus particle, known as a virion, consists of [[nucleic acid]] surrounded by a protective coat of [[protein]] called a [[capsid]]. Viruses can have a [[lipid]] "envelope" derived from the host [[cell membrane]]. A capsid is made from proteins encoded by the viral [[genome]] and its shape serves as the basis for [[morphology (biology)|morphological]] and antigenic distinction.<ref name="pmid14019094">{{cite journal
 +
|author=CASPAR DL, KLUG A
 +
 
 +
|title=Physical principles in the construction of regular viruses
 +
 
 +
|journal=Cold Spring Harb. Symp. Quant. Biol.
 +
 
 +
|volume=27
 +
 
 +
|issue=
 +
|pages=1–24
 +
 
 +
|year=1962
 +
 
 +
|pmid=14019094
 +
 
 +
|doi=
 +
}}</ref><ref name="pmid13309339">{{cite journal
 +
|author=CRICK FH, WATSON JD
 +
 
 +
|title=Structure of small viruses
 +
 
 +
|journal=Nature
 +
 
 +
|volume=177
 +
 
 +
|issue=4506
 +
 
 +
|pages=473–5
 +
 
 +
|year=1956
 +
 
 +
|pmid=13309339
 +
 
 +
|doi=
 +
}}</ref> Virally coded protein subunits will self-assemble to form a capsid, generally requiring the presence of the virus genome. However, complex viruses code for proteins which assist in the construction of their capsid.<ref name=prescott> </ref> Proteins associated with nucleic acid are known as [[nucleoprotein]]s, and the association of viral capsid proteins with viral nucleic acid is called a nucleocapsid.
  
 
In general, there are four main morphological virus types:
 
In general, there are four main morphological virus types:
  
 
{| cellpadding=3 cellspacing=0 border=1 style="border-collapse:collapse"
 
{| cellpadding=3 cellspacing=0 border=1 style="border-collapse:collapse"
|bgcolor="#dddddd"| '''Image'''
+
|colspan=2 bgcolor="#dddddd"| '''Helical viruses'''
|bgcolor="#dddddd"| '''Helical viruses'''
 
 
|-
 
|-
 
| [[Image:Tobacco mosaic virus structure.png|center|thumb|200px|Diagram of a helical capsid]]
 
| [[Image:Tobacco mosaic virus structure.png|center|thumb|200px|Diagram of a helical capsid]]
| Helical capsids are composed of a single type of subunit stacked around a central axis to form a helical structure which may have a central cavity, or hollow tube. This arrangement results in rod-shaped or filamentous virions: these can be anything from short and highly rigid, to long and very flexible. The genetic material - generally single-stranded RNA, but also ssDNA in the case of certain phages - is bound into the protein helix, by charge interactions between the negatively-charged nucleic acid and positive charges on the protein. Overall, the length of a helical capsid is related to the length of the nucleic acid contained within it, while the diameter is dependent on the size and arrangement of protomers. The well-studied [[Tobacco mosaic virus]] is an example of a helical virus.
+
| Helical capsids are composed of a single type of subunit stacked around a central axis to form a helical structure which may have a central cavity, or hollow tube. This arrangement results in rod-shaped or filamentous virions: these can be anything from short and highly rigid, to long and very flexible. The genetic material, generally single-stranded RNA, but ssDNA in some cases, is bound into the protein helix, by interactions between the negatively-charged nucleic acid and positive charges on the protein. Overall, the length of a helical capsid is related to the length of the nucleic acid contained within it and the diameter is dependent on the size and arrangement of protomers. The well-studied [[Tobacco mosaic virus]] is an example of a helical virus.
 
|-
 
|-
|bgcolor="#dddddd"| '''Image'''
+
|colspan=2 bgcolor="#dddddd"| '''Icosahedral viruses'''
|bgcolor="#dddddd"| '''Icosahedral viruses'''
 
 
|-
 
|-
| [[Image:Coronaviruses 004 lores.jpg|center|thumb|200px|Electron micrograph of icosahedral virions]]
+
| [[Image:Enteric Adenoviruses.jpg|center|thumb|200px|Electron micrograph of icosahedral virions]]
| Icosahedral capsid symmetry results in a spherical appearance of viruses at low magnification but actually consists of capsomers arranged in a regular geometrical pattern, similar to a [[football (soccer)|soccer ball]], hence they are not truly "spherical". Capsomers are ring shaped structures constructed from five to six copies of protomers. These associate via [[chemical bond|non-covalent bonding]] to enclose the viral nucleic acid, though generally less intimately than helical capsids, and may involve one or more protomers.
+
| Icosahedral capsid symmetry results in a spherical appearance of viruses at low magnification but actually consists of capsomers arranged in a regular geometrical pattern, similar to a soccer ball, hence they are not truly "spherical". Capsomers are ring shaped constructed from five to six copies of protomers. These associate via [[chemical bond|non-covalent bonding]] to enclose the viral nucleic acid, though generally less intimately than helical capsids, and may involve one or more protomers.
Icosahedral architecture was employed by [[Buckminster Fuller|R. Buckminster-Fuller]] in his [[geodesic dome]], and is the most efficient way of creating an enclosed robust structure from multiple copies of a single protein.  
+
Icosahedral architecture was employed by R. Buckminster Fuller in his geodesic dome, and is the most efficient way of creating an enclosed robust structure from multiple copies of a single protein.
The number of proteins required to form a spherical virus capsid is denoted by the T-number,<ref name="triang">{{Cite web|url=http://web.archive.org/web/20060223170529/http://rhino.bocklabs.wisc.edu/cgi-bin/virusworld/htdocs.pl?docname=triangulation.html|title=Virus triangulation numbers via Internet Archive|accessdate=2006-04-05}}</ref> where 60&times;''t'' proteins are necessary. In the case of the [[hepatitis B]] virus the T-number is 4, therefore 240 proteins assemble to form the capsid.
+
The number of proteins required to form a spherical virus capsid is denoted by the T-number,<ref name="triang">{{Cite web
 +
|url=http://web.archive.org/web/20060223170529/http://rhino.bocklabs.wisc.edu/cgi-bin/virusworld/htdocs.pl?docname=triangulation.html
 +
|title=Virus triangulation numbers via Internet Archive|accessdate=2006-04-05}}</ref> where 60&times;''t'' proteins are necessary. In the case of the [[hepatitis B]] virus the T-number is 4, and 240 proteins assemble to form the capsid.
 
|-
 
|-
|bgcolor="#dddddd"| '''Image'''
+
|colspan=2 bgcolor="#dddddd"| '''Enveloped viruses '''
|bgcolor="#dddddd"| '''Enveloped viruses '''
 
 
|-
 
|-
| [[Image:HIV Viron.png|thumb|center|200px|Diagram of enveloped [[HIV]]]]
+
| [[Image:Chickenpox-virus.jpg|thumb|center|200px|Herpes zoster virus]]
| In addition to a protein capsid many viruses are able to envelope themselves in a modified form of one of the [[cell membranes]] - the outer membrane surrounding an infected host cell, or from internal membranes such as nuclear membrane or endoplasmic reticulum - thus gaining an outer lipid bilayer known as a [[viral envelope]]. This membrane is studded with proteins coded for by the viral genome and host genome; however the lipid membrane itself and any carbohydrates present are entirely host-coded. The Influenza virus and HIV use this strategy.
+
| Viruses are able to envelope themselves in a modified form of one of the [[cell membranes]] either the outer membrane surrounding an infected host cell, or from internal membranes such as nuclear membrane or endoplasmic reticulum, thus gaining an outer lipid bilayer known as a [[viral envelope]]. This membrane is studded with proteins coded for by the viral genome and host genome; however the lipid membrane itself and any carbohydrates present are entirely host-coded. The Influenza virus and HIV use this strategy.
  
The viral envelope can give a virion a few distinct advantages over other capsid-only virions, such as protection from enzymes and certain chemicals. The proteins in it can include [[glycoprotein]]s functioning as [[receptor (biochemistry)|receptor molecules]], allowing host cells to recognise and bind these virions, resulting in the possible uptake of the virion into the cell. Most enveloped viruses are dependent upon the envelope for infectivity.
+
The viral envelope can give a virion a few distinct advantages over other capsid-only virions, such as protection from enzymes and certain chemicals. The proteins in it can include [[glycoprotein]]s functioning as [[receptor (biochemistry)|receptor molecules]], allowing host cells to recognize and bind these virions, resulting in the possible uptake of the virion into the cell. Most enveloped viruses are dependent on the envelope for infectivity.
 
|-
 
|-
|bgcolor="#dddddd"| '''Image'''
+
|colspan=2 bgcolor="#dddddd"| '''Complex viruses'''
|bgcolor="#dddddd"| '''Complex viruses'''
 
 
|-
 
|-
 
| [[Image:Tevenphage.png|thumb|center|200px|Diagram of a bacteriophage]]
 
| [[Image:Tevenphage.png|thumb|center|200px|Diagram of a bacteriophage]]
| These viruses possess a capsid which is neither purely helical, nor purely icosahedral, and which may possess extra structures such as protein tails or a complex outer wall. Some [[bacteriophages]] have a complex structure consisting of an icosahedral head bound to a helical tail, the latter of which may have a hexagonal base plate with many protruding protein tail fibres.  
+
| These viruses possess a capsid which is neither purely helical, nor purely icosahedral, and which may possess extra structures such as protein tails or a complex outer wall. Some [[bacteriophages]] have a complex structure consisting of an icosahedral head bound to a helical tail, the latter of which may have a hexagonal base plate with protruding protein tail fibres.
 +
|-
 +
| [[Image:Poxvirus.jpg|thumb|center|200px|Poxvirus]]
 +
|The [[Poxvirus]]es are large, complex viruses which have an unusual [[morphology (biology)|morphology]]. The viral genome is associated with proteins within a central disk structure known as a [[nucleoid]]. The nucleoid is surrounded by a membrane and two lateral bodies of unknown function. The virus has an outer envelope with a thick layer of protein studded over its surface. The whole particle is slightly [[pleiomorphic]], ranging from ovoid to brick shape.<ref>Long GW, Nobel J, Murphy FA, Herrmann KL, and Lourie B (1970) Experience with electron microscopy in the differential diagnosis of smallpox. Applied Microbiology 20(3):497-504.</ref>
 +
|}
  
The [[Poxvirus]]es are large, complex viruses which have an unusual [[morphology (biology)|morphology]]. The viral genome is associated with proteins within a central disk structure known as a [[nucleoid]]. The nucleoid is surrounded by a membrane and two lateral bodies of unknown function. The virus has an outer envelope with a thick layer of protein studded over its surface. The whole particle is slightly [[pleiomorphic]], ranging from ovoid to brick shape{{Fact|date=April 2007}}.
+
=== Electron microscopy ===
|}
+
{{details|Electron microscopy}}
 +
[[Image:Relative scale.svg|thumb|300px|right|The range of sizes shown by viruses, relative to those of other organisms and [[biomolecule]]s]]
 +
[[Electron microscopy]] is the most common method used to study the [[morphology (biology)|morphology]] of viruses. To increase the contrast between viruses and the background, electron-dense "stains" are used. These are solutions of salts of heavy metals such as [[tungsten]], that scatter the electrons from regions covered with the stain. When virus particles are coated with stain (positive staining), fine detail is obscured. [[Negative staining]] overcomes this problem by staining the background only.<ref name="pmid1715774">{{cite journal
 +
|author=Kiselev NA, Sherman MB, Tsuprun VL
 +
|title=Negative staining of proteins
 +
|journal=Electron Microsc. Rev.
 +
|volume=3
 +
|issue=1
 +
|pages=43–72
 +
|year=1990
 +
|pmid=1715774
 +
|doi=}}</ref>
  
[[Image:Relative scale.svg|thumb|300px|left|The range of sizes shown by viruses, relative to those of other organisms and [[biomolecule]]s]]
 
 
=== Size ===
 
=== Size ===
To put viral size into perspective, a medium sized virion next to a flea is roughly equivalent to a human next to a mountain twice the size of [[Mount Everest]]. Some [[filovirus]]es have a total length of up to 1400&nbsp;nm, however their capsid diameters are only about 80&nbsp;nm. The majority of viruses which have been studied have a [[capsid]] diameter between 10 and 300 [[nanometres]]. While most viruses are unable to be seen with a [[light microscope]], some are as large or larger than the smallest bacteria and can be seen under high optical magnification. More commonly, both scanning and transmission [[electron microscope]]s are used to visualise virus particles.
+
A medium-sized virion next to a flea is roughly equivalent to a human next to a mountain twice the size of Mount Everest. Some [[filovirus]]es have a total length of up to 1400&nbsp;nm, however their capsid diameters are only about 80&nbsp;nm. Most viruses which have been studied have a [[capsid]] diameter between 10 and 300 [[nanometres]]. Most viruses are unable to be seen with a [[light microscope]] but some are as large or larger than the smallest bacteria and can be seen under high optical magnification. More commonly, both scanning and transmission [[electron microscope]]s are used to visualize virus particles.
 
 
A notable exception to the normal viral size range is the recently discovered [[mimivirus]], with a diameter of 750&nbsp;nm which is larger than a ''[[Mycoplasma]]'' bacterium.<ref name=robertson>{{cite journal | author = Robertson J, Gomersall M, Gill P | title = Mycoplasma hominis: growth, reproduction, and isolation of small viable cells | journal = J Bacteriol. | volume = 124 | issue = 2 | pages = 1007 – 18 | year = 1975 | id = PMID 1102522}}</ref><ref name=claverie>{{cite journal | author = Claverie J, Ogata H, Audic S, Abergel C, Suhre K, Fournier P | title = Mimivirus and the emerging concept of "giant" virus | journal = Virus Res | volume = 117 | issue = 1 | pages = 133-44 | year = 2006 | pmid = 16469402}}</ref> They also hold the record for the largest viral genome size, possessing about 1000 genes (some bacteria only possess 400) on a genome approximately 1.2 [[megabase]]s in length.<ref name=raoult>{{cite journal | author = Raoult D, Audic S, Robert C, ''et al'' | title = The 1.2-megabase genome sequence of Mimivirus | journal = Science | volume = 306 | issue = 5700 | pages = 1344-50 | year = 2004 | pmid = 15486256}}</ref> Their large genome also contains many genes which are [[Homology (biology)|conserved]] in both prokaryotic and eukaryotic genes.<ref name="mimi1">{{Cite web|url=http://www.stanford.edu/group/virus/mimi/2005/Genome.htm|title=Mimiviridae genome|accessdate=2007-04-05|publisher=Stanford University}}</ref> The discovery of the virus has led many scientists to reconsider the controversial boundary between living organisms and viruses, which are currently considered as mere mobile genetic elements.
 
  
 
== Genome ==
 
== Genome ==
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! Property || Parameters
 
! Property || Parameters
 
|-
 
|-
| ''Nucleic acid'' ||  
+
| ''Nucleic acid'' ||
 
*DNA
 
*DNA
 
*RNA
 
*RNA
 
*Both DNA and RNA
 
*Both DNA and RNA
 
|-
 
|-
| ''Shape'' ||  
+
| ''Shape'' ||
 
*Linear
 
*Linear
 
*Circular
 
*Circular
Line 146: Line 365:
 
|}
 
|}
  
An enormous variety of genomic structures can be seen among viral species; as a group they contain more structural genomic diversity than the entire kingdoms of either plants, animals, or bacteria<ref name="flint">{{cite book | title=Principles of Virology| edition=2nd edn |last=Flinth| coauthors=et al.| date=2004| publisher=ASM Press, New York| id=1-55581-259-7}}</ref>.
+
An enormous variety of genomic structures can be seen among viral species; as a group they contain more structural genomic diversity than the entire kingdoms of either plants, animals, or bacteria.<ref name="flint">{{cite book | title=Principles of Virology| edition=2nd edn |last=Flinth| coauthors=et al.| date=2004| publisher=ASM Press, New York| id=1-55581-259-7}}</ref>
  
 
===Nucleic acid===
 
===Nucleic acid===
A virus may employ either [[DNA]] or [[RNA]] as the nucleic acid. Rarely do they contain both, however [[cytomegalovirus]] is an exception to this, possessing a DNA core with several [[mRNA]] segments.<ref name=prescott> </ref> Plant viruses tend to have single-stranded RNA and bacteriophages tend to have double-stranded DNA.<ref name="prescott"> </ref> Some virus species possess abnormal [[nucleotide]]s, such as ''hydroxymethylcytosine'' instead of [[cytosine]], as a normal part of their genome.<ref name="prescott"> </ref>
+
A virus may employ either [[DNA]] or [[RNA]] as the nucleic acid. Rarely do they contain both, however [[cytomegalovirus]] is an exception to this, possessing a DNA core with several [[mRNA]] segments.<ref name=prescott> </ref> By far most viruses have RNA. Plant viruses tend to have single-stranded RNA and bacteriophages tend to have double-stranded DNA.<ref name="prescott"> </ref> Some virus species possess abnormal [[nucleotide]]s, such as hydroxymethylcytosine instead of [[cytosine]], as a normal part of their genome.<ref name="prescott"> </ref>
  
 
===Shape===
 
===Shape===
Viral genomes may be circular, such as [[polyomavirus]]es, or linear, such as [[adenovirus]]es. The type of nucleic acid is irrelevant to the shape of the genome. Among [[RNA virus]]es, the genome may be divided up into separate parts within the virion, or ''segmented''. All double-stranded RNA genomes, and some single-stranded RNA genomes, are segmented.<ref name=prescott> </ref> Each segment may code for one protein, and they are usually found together in one capsid. Not all segments are required to be in the same virion for the overall virus to be infectious, as demonstrated by the [[brome mosaic virus]].<ref name="prescott"> </ref>
+
Viral genomes may be circular, such as [[polyomavirus]]es, or linear, such as [[adenovirus]]es. The type of nucleic acid is irrelevant to the shape of the genome. Among [[RNA virus]]es, the genome is often divided up into separate parts within the virion and are called ''segmented''. Double-stranded RNA genomes and some single-stranded RNA genomes are segmented.<ref name=prescott> </ref> Each segment often codes for one protein and they are usually found together in one capsid. Every segment is not required to be in the same virion for the overall virus to be infectious, as demonstrated by the [[brome mosaic virus]].<ref name="prescott"> </ref>
  
 
===Strandedness===
 
===Strandedness===
A viral genome, irrespective of nucleic acid type, may be either single-stranded or double-stranded. Single-stranded genomes consist of an unpaired nucleic acid, analogous to one-half of a ladder split down the middle. Double-stranded genomes consist of 2 complimentary paired nucleic acids, analogous to a ladder. Some viruses, such as those belonging to the ''[[Hepadnaviridae]]'', contain a genome which is partially double-stranded and partially single-stranded.<ref name="flint"> </ref>
+
A viral genome, irrespective of nucleic acid type, may be either single-stranded or double-stranded. Single-stranded genomes consist of an unpaired nucleic acid, analogous to one-half of a ladder split down the middle. Double-stranded genomes consist of 2 complementary paired nucleic acids, analogous to a ladder. Viruses, such as those belonging to the ''[[Hepadnaviridae]]'', contain a genome which is partially double-stranded and partially single-stranded.<ref name="flint"> </ref> Viruses that infect humans include double-stranded RNA (e.g. [[Rotavirus]]), single-stranded RNA (e.g. [[Influenza virus]]), single-stranded DNA (e.g. [[Parvovirus B19]]) and double-stranded DNA ([[Herpesviridae|Herpes virus]]).
  
 
===Sense===
 
===Sense===
For viruses with RNA as their nucleic acid, the strands are said to be either [[positive-sense]] (also called plus-strand) or [[negative-sense]] (also called minus-strand) depending on whether it is complementary to viral mRNA. Positive-sense viral RNA is identical to viral mRNA and thus can be immediately [[translation (genetics)|translated]] by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an [[RNA polymerase]] before translation. DNA nomenclature is similar to RNA nomenclature, in that the ''coding strand'' for the viral mRNA is complementary to it (-), and the ''non-coding strand'' is a copy of it (+).
+
For viruses with RNA as their nucleic acid, the strands are said to be either [[positive-sense]] (called the plus-strand) or [[negative-sense]] (called the minus-strand), depending on whether it is complementary to viral mRNA. Positive-sense viral RNA is identical to viral mRNA and thus can be immediately [[translation (genetics)|translated]] by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an [[RNA polymerase]] before translation. DNA nomenclature is similar to RNA nomenclature, in that the ''coding strand'' for the viral mRNA is complementary to it (-), and the ''non-coding strand'' is a copy of it (+).
  
 
===Genome size===
 
===Genome size===
Genome size in terms of the weight of [[nucleotides]] varies between species. The smallest genomes code for only four proteins and weigh about 10<sup>6</sup> [[Atomic mass unit|dalton]]s, while the largest weigh about 10<sup>8</sup> daltons and code for over one hundred proteins.<ref name=prescott> </ref> [[RNA virus]]es generally have smaller genome sizes than [[DNA virus]]es due to a higher error-rate when replicating, resulting in a maximum upper size limit. Beyond this limit, too many errors in the genome when replicating render the virus useless or uncompetitive. In contrast, DNA viruses generally have larger genomes due to the high fidelity of their replication enzymes.<ref name="flint"> </ref>
+
Genome size in terms of the weight of [[nucleotides]] varies between species. The smallest genomes code for only four proteins and weigh about 10<sup>6</sup> [[Atomic mass unit|Daltons]], the largest weigh about 10<sup>8</sup> Daltons and code for over one hundred proteins.<ref name=prescott> </ref> [[RNA virus]]es generally have smaller genome sizes than [[DNA virus]]es due to a higher error-rate when replicating, resulting in a maximum upper size limit. Beyond this limit, errors in the genome when replicating render the virus useless or uncompetitive. To compensate for this, RNA viruses often have segmented genomes where the genome is split into smaller molecules, thus reducing the chance of error.<ref>Pressing J, Reanney DC. Divided genomes and intrinsic noise.J Mol Evol. 1984;20(2):135-46.</ref> In contrast, DNA viruses generally have larger genomes due to the high fidelity of their replication enzymes.<ref name="flint"> </ref>
  
==Replication==
+
===Gene reassortment===
Viral populations do not grow through [[cell division]], because they are acellular; instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves. A virus can still cause degenerative effects within a cell without causing its death; collectively these are termed '''[[cytopathic effect]]s'''. Released virions can be passed between hosts through either direct contact, often via [[body fluids]], or through a [[vector (biology)|vector]]. In aqueous environments, viruses float free in the water.
+
There is an evolutionary advantage in having a segmented genome. Different strains of a virus with a segmented genome, from a pig or a bird or a human for example, such as [[Influenza virus]], can shuffle and combine with other genes producing progeny viruses or (offspring) that have unique characteristics. This is called reassortment or ''viral sex''.<ref> Goudsmit, Jaap. Viral Sex. Oxford Univ Press, 1998.ISBN-13: 9780195124965 ISBN-10: 0195124960</ref> This is one reason why Influenza virus constantly changes.<ref> Zhou NN, Senne DA, Landgraf JS, Swenson SL, Erickson G, Rossow K, Liu L, Yoon K, Krauss S, Webster RG. Genetic reassortment of avian, swine, and human influenza A viruses in American pigs.J Virol. 1999 Oct;73(10):8851-6.</ref>
  
===Lytic or lysogenic===
+
===Genetic recombination===
Viruses may have a [[lytic cycle|lytic]] or a [[lysogenic cycle]], with some viruses capable of carrying out both.<ref name=prescott> </ref>
+
[[Genetic recombination]] is the process by which a strand of DNA is broken and then joined to the end of a different DNA molecule. This can occur when viruses infect cells simultaneously and studies of viral evolution have shown that recombination has been rampant in the species studied.<ref name="pmid10573145">{{cite journal
 +
|author=Worobey M, Holmes EC
 +
|title=Evolutionary aspects of recombination in RNA viruses
 +
|journal=J. Gen. Virol.
 +
|volume=80 ( Pt 10)
 +
|issue=
 +
|pages=2535–43
 +
|year=1999
 +
|pmid=10573145
 +
|doi=}}</ref> Recombination is common to both RNA and DNA viruses.<ref name="pmid15578739">{{cite journal
 +
|author=Lukashev AN
 +
|title=Role of recombination in evolution of enteroviruses
 +
|journal=Rev. Med. Virol.
 +
|volume=15
 +
|issue=3
 +
|pages=157–67
 +
|year=2005
 +
|pmid=15578739
 +
|doi=10.1002/rmv.457}}</ref><ref name="pmid10479778">{{cite journal
 +
|author=Umene K
 +
|title=Mechanism and application of genetic recombination in herpesviruses
 +
|journal=Rev. Med. Virol.
 +
|volume=9
 +
|issue=3
 +
|pages=171–82
 +
|year=1999
 +
|pmid=10479778
 +
|doi=}}</ref>
  
====Lytic cycle====
+
===Genetic change===
{{Main|Lytic cycle}}
+
Viruses undergo genetic change by several mechanisms. These include a process called [[genetic drift]] where individual bases in the DNA or RNA [[mutate]] to other bases. Most of these [[point mutations]] are silent in that they do not change the protein that the gene encodes, but others can confer evolutionary advantages such as resistance to [[antiviral drugs]].<ref>Pan XP, Li LJ, Du WB, Li MW, Cao HC, Sheng JF. Differences of YMDD mutational patterns, precore/core promoter mutations, serum HBV DNA levels in lamivudine-resistant hepatitis B genotypes B and C. J Viral Hepat. 2007 Nov;14(11):767-74.</ref> [[Antigenic shift]] is where there is a major change in the [[genome]] of the virus. This occurs as a result of [[Genetic recombination|recombination]] or [[reassortment]] (see above). When this happens with [[influenza]] viruses, [[pandemics]] may result.<ref>Hampson AW, Mackenzie JS. The influenza viruses.Med J Aust. 2006 Nov 20;185(10 Suppl):S39-43.</ref><ref>Nakajima K. The mechanism of antigenic shift and drift of human influenza virus Nippon Rinsho. 2003 Nov;61(11):1897-903.</ref> By genome rearrangement the structure of the gene changes although no mutations have necessarily occurred.<ref>Hundley F, McIntyre M, Clark B, Beards G, Wood D, Chrystie I, Desselberger U. Heterogeneity of genome rearrangements in rotaviruses isolated from a chronically infected immunodeficient child.J Virol. 1987 Nov;61(11):3365-72.</ref>
In the lytic cycle, characteristic of virulent phages such as the [[T4 phage]], host cells will be induced by the virus to begin manufacturing the proteins necessary for virus reproduction. As well as proteins, the virus must also direct the replication of new genomes, the technique used for this varies greatly between virus species but depends heavily on the genome type. The final viral product is assembled spontaneously, though it may be aided by [[chaperone|molecular chaperone]]s. After the genome has been replicated and the new capsid assembled, the virus causes the cell to be broken open (lysed) to release the virus particles. Some viruses do not lyse the cell but instead exit the cell via the [[cell membrane]] in a process known as [[exocytosis]], taking a small portion of the membrane with them as a viral envelope. As soon as the cell is destroyed the viruses have to find a new host.  
 
  
====Lysogenic cycle====
+
RNA viruses are much more likely to mutate than DNA viruses for the reasons outlined above. Viruses often exist as quasispecies or swarms of viruses of the same species but with slightly different genome nucleoside sequences. Such quasispecies are a prime target for [[natural selection]].<ref>Metzner KJ. Detection and significance of minority quasispecies of drug-resistant HIV-1. HIV Ther. 2006 Dec;11(4):74-81.</ref>
{{Main|Lysogenic cycle}}
 
In contrast, the lysogenic cycle does not result in immediate lysing of the host cell, instead the viral genome integrates into the host DNA and replicates along with it. The virus remains dormant but after the host cell has replicated several times, or if environmental conditions permit it, the virus will become active and enter the lytic phase. The lysogenic cycle allows the host cell to continue to survive and reproduce, and the virus is passed on to all of the cell’s offspring.
 
  
[[Image:Bacteriophage.jpg|thumb|200px|right|A falsely coloured electron micrograph of multiple [[bacteriophage]]s]]
+
==Replication==
 +
Viral populations do not grow through [[cell division]], because they are acellular; instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves. A virus can still cause degenerative effects within a cell without causing its death; collectively these are termed [[cytopathic effect]]s.
 +
===Virus life cycle===
 +
The [[viral life cycle|life cycle of viruses]] differs greatly between species (see below) but there are six ''basic'' stages in the life cycle of viruses:
 +
[[Image:Virus Replication.svg|right|thumb|250px|A virus attaches to the host cell and enters endocytosis. The capsid protein dissociates and the viral RNA is transported to the nucleus. In the nucleus, the viral polymerase complexes transcribe and replicate the RNA. Viral mRNAs migrate to cytoplasm where they are translated into protein. Then the newly synthesized virions [[viral shedding|bud]] from infected cell.]]
 +
*'''Attachment''' is a specific binding between viral capsid proteins and specific receptors on the host cellular surface. This specificity determines the host range of a virus. For example, the human immunodeficiency virus ([[HIV]]) infects only human [[T cells]], because its surface protein, [[gp120]], can interact with [[CD4]] and receptors on the T cell's surface. This mechanism has evolved to favour those viruses that only infect cells that they are capable of replicating in. Attachment to the receptor can induce the viral-envelope protein to undergo changes that results in the fusion of viral and cellular membranes.
 +
*'''Penetration''': following attachment, viruses enter the host cell through receptor mediated [[endocytosis]] or membrane fusion.
 +
*'''Uncoating''' is a process in which the viral [[capsid]] is degraded by viral [[enzymes]] or host enzymes thus releasing the viral genomic nucleic acid.
 +
*'''Replication''' involves synthesis of viral messenger RNA ([[mRNA]]) for viruses except positive sense RNA viruses (see above), viral [[Protein biosynthesis|protein synthesis]] and assembly of viral proteins and viral genome replication.
 +
*Following the '''assembly''' of the virus particles post-translational modification of the viral proteins often occurs. In viruses such as [[HIV]], this modification, (sometimes called maturation), occurs ''after'' the virus has been released from the host cell.<ref name="pmid11451488">{{cite journal
 +
|author=Barman S, Ali A, Hui EK, Adhikary L, Nayak DP
 +
|title=Transport of viral proteins to the apical membranes and interaction of matrix protein with glycoproteins in the assembly of influenza viruses
 +
|journal=Virus Res.
 +
|volume=77
 +
|issue=1
 +
|pages=61–9
 +
|year=2001
 +
|pmid=11451488
 +
|doi=}}</ref>
 +
*Viruses are released from the host cell by lysis (see below). Enveloped viruses (e.g., HIV) typically are released from the host cell by [[viral shedding|budding]]. During this process, the virus acquires its phospholipid envelope which contains embedded viral glycoproteins.
  
===Bacteriophages===
+
====DNA viruses====
'''[[Bacteriophage]]s''' infect specific bacteria by binding to [[receptor (biochemistry)|surface receptor molecule]]s and then enter the cell. Within a short amount of time, sometimes just minutes, bacterial [[polymerase]] starts translating viral mRNA into protein. These proteins go on to become either new virions within the cell, helper proteins which help assembly of new virions, or proteins involved in cell [[lysis]]. Viral enzymes aid in the breakdown of the cell membrane, and in the case of the [[T4 phage]], in just over twenty minutes after injection over three hundred phages will be released.
+
Animal [[DNA virus]]es, such as [[herpesvirus]]es, enter the host via [[endocytosis]], the process by which cells take in material from the external environment. Frequently after a chance collision with an appropriate surface receptor on a cell, the virus penetrates the cell, the viral genome is released from the capsid, and host polymerases begin transcribing viral mRNA. New virions are assembled and released either by cell lysis or by [[viral shedding|budding]] off the cell membrane.
  
===DNA viruses===
+
====RNA viruses====
Animal '''[[DNA virus]]es''', such as [[herpesvirus]]es, enter the host via [[endocytosis]], the process by which cells take in material from the external environment. Frequently after a chance collision with an appropriate surface receptor on a cell, the virus penetrates the cell, the viral genome is released from the capsid and host polymerases begin transcribing viral mRNA. New virions are assembled and released either by cell lysis or by budding off the cell membrane.
+
Animal [[RNA viruses]] can be placed into about four different groups depending on their modes of replication. The [[Sense (molecular biology)|polarity]] of the RNA largely determines the replicative mechanism, as well as whether the genetic material is single-stranded or double-stranded. Some [[RNA virus]]es are actually DNA-based but use an RNA-intermediate to replicate. RNA viruses are dependent on virally encoded [[RNA replicase]] to create copies of their genomes.
  
===RNA viruses===
+
====Reverse transcribing viruses====
Animal '''[[RNA viruses]]''' can be placed into about four different groups depending on their mode of replication. The [[Sense (molecular biology)|polarity]] of the RNA largely determines the replicative mechanism, as well as whether the genetic material is single-stranded or double-stranded. Some [[RNA virus]]es are actually DNA based but use an RNA-intermediate to replicate. RNA viruses are heavily dependent upon virally encoded [[RNA replicase]] to create copies of their genomes.
+
[[Reverse transcribing viruses]] replicate using reverse transcription, which is the formation of DNA from an RNA template. Reverse transcribing viruses containing RNA genomes use a DNA intermediate to replicate, whereas those containing DNA genomes use an RNA intermediate during genome replication. Both types use the [[reverse transcriptase]] enzyme to carry out the nucleic acid conversion. Both types are susceptible to [[antiviral drug]]s that inhibit the reverse transcriptase enzyme, e.g. [[zidovudine]] and [[lamivudine]].
  
===Reverse transcribing viruses===
+
An example of the first type is [[HIV]] which is a [[retrovirus]]. Retroviruses often integrate the DNA produced by [[reverse transcription]] into the host genome. This is why HIV infection can at present, only be treated and not cured.
'''[[Reverse transcribing viruses]]''' are viruses that replicate using reverse transcription, which is the formation of DNA from an RNA template. Those viruses containing RNA genomes use a DNA intermediate to replicate, whereas those containing DNA genomes use an RNA intermediate during genome replication. Both types of reverse transcribing viruses use the [[reverse transcriptase]] enzyme to carry out the nucleic acid conversion.
+
 
 +
Examples of the second type are the [[Hepadnaviridae]], which includes the [[Hepatitis B]] virus and the [[Caulimoviridae]] - e.g. [[Cauliflower mosaic virus]].
 +
 
 +
====Bacteriophages====
 +
{{Main|Bacteriophage}}
 +
[[Image:Phage.jpg|thumb|150px|right|Transmission electron micrograph of multiple [[bacteriophage]]s attached to a bacterial cell wall]]
 +
[[Bacteriophage]]s infect specific bacteria by binding to [[receptor (biochemistry)|surface receptor molecules]] and then enter the cell. Within a short amount of time, in some cases, just minutes, bacterial [[polymerase]] starts translating viral mRNA into protein. These proteins go on to become either new virions within the cell, helper proteins which help assembly of new virions, or proteins involved in cell [[lysis]]. Viral enzymes aid in the breakdown of the cell membrane, and in the case of the [[T4 phage]], in just over twenty minutes after injection over three hundred phages could be released.
  
 
==Lifeform debate==
 
==Lifeform debate==
[[Image:Rotavirus TEM B82-0337 lores.jpg|thumb|200px|right|Multiple [[rotavirus]] virions]]
+
Viruses have been described as "organisms at the edge of life",<ref>Rybicki ''ibid''</ref> but argument continues over whether viruses are truly alive. According to the United States Code they are considered [[microorganism]]s in the sense of biological weaponry and malicious use. Scientists, however, are divided. Things become more complicated as they look at [[viroids]] and [[prions]]. Viruses resemble other organisms in that they possess genes and can evolve in infected cells by [[natural selection]].<ref>Holmes EC.PLoS Biol. 2007 Oct 2;5(10):e278. Viral Evolution in the Genomic Age</ref><ref>Shackelton LA, Holmes EC.Phylogenetic evidence for the rapid evolution of human B19 erythrovirus.J Virol. 2006 Apr;80(7):3666-9.</ref>
Argument continues over whether viruses are truly alive. According to the [[United States Code]], they are considered [[microorganism]]s in the sense of biological weaponry and malicious use. Scientists, however, are divided. Things become complicated as they look at simple viruses, [[viroids]] and [[prions]]. Viruses resemble other organisms in that they possess nucleic acid, and can respond - in infected cells - to their environment in a limited fashion. They can also reproduce by creating multiple copies of themselves through simple self-assembly.
+
They can reproduce by creating multiple copies of themselves through self-assembly.
  
Viruses do not have a [[cell (biology)|cell]] structure, regarded as the basic unit of life. Additionally, although they reproduce, they do not metabolise on their own and therefore require a host cell to replicate and synthesise new products. Bacterial species such as [[Rickettsia]] and [[Chlamydia]], while living organisms, are even unable to reproduce outside of a host cell.
+
Viruses do not have a [[cell (biology)|cell]] structure (regarded as the basic unit of life), although they do have genes. Additionally, although they reproduce, they do not self-metabolize and require a host cell to replicate and synthesize new products. However, bacterial species such as [[Rickettsia]] and [[Chlamydia]] are considered living organisms but are unable to reproduce outside a host cell.
  
An argument can be made that all accepted forms of life use [[cell division]] to reproduce, whereas all viruses spontaneously assemble within cells. The comparison is drawn between viral self-assembly and the autonomous growth of non-living [[crystallization|crystal]]s. Virus self-assembly within host cells also has implications for the study of the [[origin of life]], as it lends credence to the hypothesis that life could have started as self-assembling organic molecules{{Fact|date=April 2007}}.
+
An argument can be made that accepted forms of life use [[cell division]] to reproduce, whereas viruses spontaneously assemble within cells. The comparison is drawn between viral self-assembly and the autonomous growth of non-living [[crystallization|crystals]]. Virus self-assembly within host cells has implications for the study of the [[origin of life]], as it lends credence to the hypothesis that life could have started as self-assembling organic molecules.<ref>Vlassov, Alexander V. (Jul 2005). "The RNA World on Ice: A New Scenario for the Emergence of RNA Information". Journal of Molecular Evolution 61: 264-273. </ref>
  
If viruses are considered alive, then the criteria specifying life will have been permanently changed, leading scientists to question what the basic prerequisite of life is. The standards required to call something artificially alive would be reduced and the prospect of creating [[artificial life]] would be enhanced. If viruses were said to be alive, the question could follow of whether even smaller infectious particles, such as [[viroid]]s and [[prion]]s, are alive.
+
If viruses are considered alive, then the criteria specifying life will have to exclude the cell. If viruses are said to be alive, the question could follow of whether even smaller infectious particles, such as [[viroid]]s and [[prion]]s, are alive.
  
 
==Viruses and disease==
 
==Viruses and disease==
:''For more examples of diseases caused by viruses see [[List of infectious diseases]]
+
:''For more examples of diseases caused by viruses see [[List of infectious diseases]].
Examples of common human diseases caused by viruses include the [[common cold]], [[influenza|the flu]], [[chickenpox]] and [[cold sores]]. Many serious diseases such as [[Ebola]], [[AIDS]], [[avian flu]] and [[SARS]] are also caused by viruses. The relative ability of viruses to cause disease is described in terms of [[virulence]]. Other diseases are under investigation as to whether they too have a virus as the causative agent, such as the possible connection between [[Human Herpesvirus Six]] (HHV6) and neurological diseases such as [[multiple sclerosis]] and [[chronic fatigue syndrome]]. Recently it was also shown that cervical cancer is partially caused by [[papillomavirus]], representing evidence in humans of a link existing between cancer and an infective agent.<ref name=BBC_1999>{{cite news | title=Human Papilloma Virus |url=http://news.bbc.co.uk/2/hi/health/medical_notes/429762.stm |publisher = BBC News |date=1999-08-26 |accessdate=2007-03-17 }}</ref> There is current controversy over whether the [[borna virus]], previously thought of as causing [[neurology|neurological]] disease in horses, could be responsible for [[psychiatry|psychiatric]] illness in humans.<ref name=Chen_1999>{{cite journal |author=Chen C, Chiu Y, Wei F, Koong F, Liu H, Shaw C, Hwu H, Hsiao K |title=High seroprevalence of Borna virus infection in schizophrenic patients, family members and mental health workers in Taiwan |journal=Mol Psychiatry |volume=4 |issue=1 |pages=33-8 |year=1999 |pmid=10089006}}</ref>
+
Examples of common human diseases caused by viruses include the [[common cold]], [[influenza|the flu]], [[chickenpox]] and [[cold sores]]. Serious diseases such as [[Ebola]], [[AIDS]], [[avian influenza]] and [[SARS]] are caused by viruses. The relative ability of viruses to cause disease is described in terms of [[virulence]]. Other diseases are under investigation as to whether they too have a virus as the causative agent, such as the possible connection between [[Human Herpesvirus Six]] (HHV6) and neurological diseases such as [[multiple sclerosis]] and [[chronic fatigue syndrome]]. There is current controversy over whether the [[borna virus]], previously thought of as causing [[neurology|neurological]] diseases in horses, could be responsible for [[psychiatry|psychiatric]] illnesses in humans.<ref name=Chen_1999>{{cite journal
 +
|author=Chen C, Chiu Y, Wei F, Koong F, Liu H, Shaw C, Hwu H, Hsiao K
 +
|title=High seroprevalence of Borna virus infection in schizophrenic patients, family members and mental health workers in Taiwan
 +
|journal=Mol Psychiatry
 +
|volume=4
 +
|issue=1
 +
|pages=33-8
 +
|year=1999
 +
|pmid=10089006
 +
}}</ref>
 +
 
 +
Viruses have different mechanisms by which they produce disease in an organism, which largely depends on the species. Mechanisms at the cellular level primarily include cell [[lysis]], the breaking open and subsequent death of the cell. In [[multicellular organism]]s, if enough cells die the whole organism will start to suffer the effects. Although viruses cause disruption of healthy [[homeostasis]], resulting in disease, they may exist relatively harmlessly within an organism. An example would include the ability of the [[herpes simplex virus]], which cause cold sores, to remain in a dormant state within the human body. This is called latency<ref>Margolis TP, Elfman FL, Leib D, Pakpour N, Apakupakul K, Imai Y, Voytek C. Spontaneous reactivation of herpes simplex virus type 1 in latently infected
 +
murine sensory Ganglia.J Virol. 2007 Oct;81(20):11069-74. Epub 2007 Aug 8.</ref> and is a characteristic of the [[herpes viruses]] including the [[Epstein-Barr virus]], which causes glandular fever, and the [[Varicella zoster]] virus, which causes [[chicken pox]]. Latent chickenpox infections return in later life as the disease called [[shingles]].
  
Viruses have many different mechanisms by which they produce disease in an organism, which largely depends on the species. Mechanisms at the cellular level primarily include cell [[lysis]], the breaking open and subsequent death of the cell. In [[multicellular organism]]s, if enough cells die the whole organism will start to suffer the effects. Although many viruses result in the disruption of healthy [[homeostasis]], resulting in disease, they may also exist relatively harmlessly within an organism. An example would include the ability of the [[herpes simplex virus]], which cause [[coldsore]]s, to remain in a dormant state within the human body.
+
Some viruses can cause life-long or [[Chronic (medical)|chronic]] infections, where the viruses continue to replicate in the body despite the hosts' defense mechanisms.<ref name="pmid17931183">{{cite journal
 +
|author=Bertoletti A, Gehring A
 +
|title=Immune response and tolerance during chronic hepatitis B virus infection
 +
|journal=Hepatol. Res.
 +
|volume=37 Suppl 3
 +
|issue=
 +
|pages=S331–8
 +
|year=2007
 +
|pmid=17931183
 +
|doi=10.1111/j.1872-034X.2007.00221.x
 +
}}</ref> This is common in [[Hepatitis B virus]] and [[Hepatitis C Virus]] infections. People chronically infected with the Hepatitis B virus are known as carriers who serve as reservoirs of infectious virus. In some populations, with a high proportion of carriers, the disease is said to be [[Endemic (epidemiology)|endemic]].<ref name="pmid17645465">{{cite journal
 +
|author=Nguyen VT, McLaws ML, Dore GJ
 +
|title=Highly endemic hepatitis B infection in rural Vietnam
 +
|journal=
 +
|volume=
 +
|issue=
 +
|pages=
 +
|year=2007
 +
|pmid=17645465
 +
|doi=10.1111/j.1440-1746.2007.05010.x}}</ref> When diagnosing Hepatitis B virus infections, it is important to distinguish between [[Acute (medical)|acute]] and [[Chronic (medical)|chronic]] infections.<ref name="pmid17664817">{{cite journal
 +
|author=Rodrigues C, Deshmukh M, Jacob T, Nukala R, Menon S, Mehta A
 +
|title=Significance of HBV DNA by PCR over serological markers of HBV in acute and chronic patients
 +
|journal=Indian journal of medical microbiology
 +
|volume=19
 +
|issue=3
 +
|pages=141–4
 +
|year=2001
 +
|pmid=17664817
 +
|doi=}}</ref>
 +
===Epidemiology===
 +
Viral [[epidemiology]] is the branch of medical science dealing with the transmission and control of virus infections in humans. Transmission of viruses can be vertical, that is from mother to child, or horizontal, which means from person to person. Examples of [[vertical transmission]] include [[Hepatitis B virus]] and [[HIV]] where the baby is born already infected with the virus.<ref name="pmid17825648">{{cite journal
 +
|author=Fowler MG, Lampe MA, Jamieson DJ, Kourtis AP, Rogers MF
 +
|title=Reducing the risk of mother-to-child human immunodeficiency virus transmission: past successes, current progress and challenges, and future directions
 +
|journal=Am. J. Obstet. Gynecol.
 +
|volume=197
 +
|issue=3 Suppl
 +
|pages=S3–9
 +
|year=2007
 +
|pmid=17825648
 +
|doi=10.1016/j.ajog.2007.06.048}}</ref> Another, more rare, example is the [[Varicella zoster virus]], which although causing relatively mild infections in humans, can be fatal to the foetus and newly born baby.<ref name="pmid11190597">{{cite journal
 +
|author=Sauerbrei A, Wutzler P
 +
|title=The congenital varicella syndrome
 +
|journal=Journal of perinatology : official journal of the California Perinatal Association
 +
|volume=20
 +
|issue=8 Pt 1
 +
|pages=548–54
 +
|year=2000
 +
|pmid=11190597
 +
|doi=}}</ref>
 +
[[Horizontal transmission]] is the most common mechanism of spread of viruses in populations. Transmission can be exchange of blood by sexual activity, e.g. [[HIV]], [[Hepatitis B]] and [[Hepatitis C]]; by mouth by exchange of [[saliva]], e.g. [[Epstein-Barr virus]], or from contaminated food or water, e.g. [[Norovirus]]; by breathing in viruses in the form of [[aerosol]]s, e.g. [[Influenza virus]]; and by insect vectors such as mosquitoes, e.g. [[dengue]].
 +
The rate or speed of transmission of viral infections depends on factors that include [[population density]], the number of susceptible individuals, (i.e. those who are not immune),<ref> Garnett GP. Role of herd immunity in determining the effect of vaccines against sexually transmitted disease.J Infect Dis. 2005 Feb 1;191 Suppl 1:S97-106.</ref> the quality of health care and the weather.<ref name="pmid16544901">{{cite journal
 +
|author=Platonov AE
 +
|title=[[The influence of weather conditions on the epidemiology of vector-borne diseases by the example of West Nile fever in Russia]] |language=Russian
 +
|journal=Vestn. Akad. Med. Nauk SSSR
 +
|volume=
 +
|issue=2
 +
|pages=25–9
 +
|year=2006
 +
|pmid=16544901
 +
|doi=}}</ref>
  
=== Epidemics ===
+
=== Epidemics and pandemics ===
[[Image:Ebola Virus TEM PHIL 1832 lores.jpg|thumb|200px|right|The [[Ebola]] virus]]
 
[[Image:Marburg virions TEM 275 lores.jpg|thumb|200px|right|The [[Marburg virus]]]]
 
 
{{details|List of epidemics}}
 
{{details|List of epidemics}}
A number of highly lethal viral pathogens are members of the [[Filoviridae]]. Filoviruses are filament-like viruses that cause [[viral hemorrhagic fever]], and include the [[Ebola]] and [[Marburg virus]]es. The Marburg virus attracted widespread press attention in April 2005 for an outbreak in [[Angola]]. Beginning in October 2004 and continuing into 2005, the outbreak was the world's worst epidemic of any kind of viral hemorrhagic fever.<ref name="bbc">{{cite web| url=http://news.bbc.co.uk/2/hi/africa/4397891.stm| title=Marburg outbreak worst recorded| date = 2005-03-31 | accessdate=2007-04-05| publisher=BBC News}}</ref>
+
[[Image:Reconstructed Spanish Flu Virus.jpg|thumb|250px|right|The reconstructed [[1918 influenza]] virus]]
 +
Native American populations were devastated by contagious diseases, particularly [[smallpox]], brought to the Americas by European colonists. It is unclear how many Native Americans were killed by foreign diseases after the arrival of Columbus in the Americas, but the numbers have been estimated to be close to 70% of the indigenous population. The damage done by this disease significantly aided European attempts to displace and conquer the native population.<ref>Ranlet P. The British, the Indians, and smallpox: what actually happened at Fort Pitt in 1763? Pa Hist. 2000;67(3):427-41.</ref><ref>Van Rijn K. "Lo! The poor Indian!" colonial responses to the 1862-63 smallpox epidemic inBritish Columbia and Vancouver Island.Can Bull Med Hist. 2006;23(2):541-60.</ref><ref>Patterson KB, Runge T. Smallpox and the Native American.Am J Med Sci. 2002 Apr;323(4):216-22.</ref><ref>Sessa R, Palagiano C, Scifoni MG, di Pietro M, Del Piano M.
 +
The major epidemic infections: a gift from the Old World to the New?
 +
Panminerva Med. 1999 Mar;41(1):78-84.</ref><ref>Bianchine PJ, Russo TA.
 +
The role of epidemic infectious diseases in the discovery of America.
 +
Allergy Proc. 1992 Sep-Oct;13(5):225-32.</ref><ref>Hauptman LM.
 +
Smallpox and American Indian; Depopulation in Colonial New York.
 +
N Y State J Med. 1979 Nov;79(12):1945-9.</ref><ref>Fortuine R.
 +
Smallpox decimates the Tlingit (1787).
 +
Alaska Med. 1988 May-Jun;30(3):109.</ref>
 +
 
 +
{{main|Spanish flu}}
 +
 
 +
A [[pandemic]] is a world-wide epidemic. The 1918 flu pandemic, commonly referred to as the [[Spanish flu]], was a [[Pandemic Severity Index|category 5]] influenza pandemic caused by an unusually severe and deadly [[Influenza A virus]]. The victims were often healthy young adults, in contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients.
 +
<br />The [[Spanish flu]] pandemic lasted from 1918 to 1919. Older estimates say it killed 40–50 million people,<ref name=Patterson1>{{cite journal
 +
| last =Patterson | first = KD | coauthors = Pyle GF | title=The geography and mortality of the 1918 influenza pandemic. | journal= Bull Hist Med. | year=1991 | month=Spring | volume=65 | issue=1 | pages = 4–21 | id = PMID 2021692}}</ref> while more recent research suggests that it may have killed as many as 100 million people, or 5% of the world's population in 1918.<ref>Johnson, Niall P. A. S. and Mueller, Juergen, "Updating the Accounts:
 +
Global Mortality of the 1918–1920 'Spanish' Influenza Pandemic," Bulletin of the History of Medicine 76 (2002), pp. 105–115.</ref>
 +
 
 +
{{main|AIDS}}
 +
 
 +
[[Image:Ebola Virus TEM PHIL 1832 lores.jpg|thumb|250px|right|The [[Ebola]] virus]]
 +
Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century;<ref name=Gao>
 +
{{ cite journal
 +
| author=Gao, F., Bailes, E., Robertson, D. L., Chen, Y., Rodenburg, C. M., Michael, S. F., Cummins, L. B., Arthur, L. O., Peeters, M., Shaw, G. M., Sharp, P. M. and Hahn, B. H.
 +
| title=Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes
 +
| journal=Nature
 +
| year=1999
 +
| pages=436&ndash;441
 +
| volume=397
 +
| issue=6718
 +
| id={{PMID |9989410}} {{doi|10.1038/17130}}
 +
}}</ref> it is now a [[pandemic]], with an estimated 38.6 million people now living with the disease worldwide.<ref name=UNAIDS2006>{{
 +
cite book
 +
| author =[[UNAIDS]]
 +
| year = 2006
 +
| title = 2006 Report on the global AIDS epidemic
 +
| chapter = Overview of the global AIDS epidemic
 +
| chapterurl = http://data.unaids.org/pub/GlobalReport/2006/2006_GR_CH02_en.pdf
 +
| accessdate = 2006-06-08
 +
| format= PDF
 +
}}</ref> As of January 2006, the [[Joint United Nations Programme on HIV/AIDS]] (UNAIDS) and the [[World Health Organization]] (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on June 5, 1981, making it one of the most destructive [[epidemic]]s in recorded history.<ref> Mawar N, Saha S, Pandit A, Mahajan U.
 +
The third phase of HIV pandemic: social consequences of HIV/AIDS stigma &
 +
discrimination & future needs.Indian J Med Res. 2005 Dec;122(6):471-84. Review.</ref>
 +
[[Image:Marburg virions TEM 275 lores.jpg|thumb|250px|right|The [[Marburg virus]]]]
  
[[Indigenous peoples of the Americas|Native American]] populations were devastated by contagious diseases, particularly [[smallpox]], brought to the Americas by European colonists. It is unclear how many Native Americans were killed by foreign diseases after the arrival of Columbus in the Americas, but the numbers have been estimated to be close to 70% of the indigenous population.<ref name="smallpoxhistory">{{cite web|url=http://www.historylink.org/essays/output.cfm?file_id=5100|title=Smallpox epidemic ravages Native Americans on the northwest coast of North America in the 1770s|accessdate=2007-04-05|publisher=HistoryLink.org}}</ref> The damage done by this disease may have significantly aided European attempts to displace or conquer the native population.
+
{{main|Ebola}}
  
=== Detection, purification and diagnosis ===
+
Several highly lethal viral pathogens are members of the [[Filoviridae]]. Filoviruses are filament-like viruses that cause [[viral hemorrhagic fever]], and include the [[Ebola]] and [[Marburg virus]]es. The Marburg virus attracted widespread press attention in April 2005 for an outbreak in Angola. Beginning in October 2004 and continuing into 2005, the outbreak was the world's worst epidemic of any kind of viral hemorrhagic fever.<ref>Towner JS, Khristova ML, Sealy TK, Vincent MJ, Erickson BR, Bawiec DA, HartmanAL, Comer JA, Zaki SR, Stroher U, Gomes da Silva F, del Castillo F, Rollin PE,Ksiazek TG, Nichol ST.
In the laboratory, several techniques for growing and detecting viruses exist. Purification of viral particles can be achieved using [[differential centrifugation]], [[isopycnic centrifugation]], precipitation with [[ammonium sulfate]] or [[ethylene glycol]], and removal of cell components from a homogenised cell mixture using [[organic solvent]]s or [[enzyme]]s to leave the virus particles in solution.
+
Marburgvirus genomics and association with a large hemorrhagic fever outbreak in
 +
Angola.J Virol. 2006 Jul;80(13):6497-516.</ref>
  
Assays to detect and quantify viruses include:
+
=== Viruses and cancer ===
[[Image:Plaque assay macro.jpg|thumb|right|A [[viral plaque]] [[assay]]]]
+
{{details|Oncovirus}}
* [[Hemagglutination assay]]s, which quantitatively measure how many virus particles are in a solution of [[red blood cells]] by the amount of [[Agglutination (biology)|agglutination]] the viruses cause between them. This occurs as many viruses are able to bind to the surface of one or more red blood cells.
+
[[Image:Leukemia cells that contain Epstein Barrvirus using a FA staining technique PHIL 2984 lores.jpg|right|thumb|250px|Human leukaemia cells infected by the [[Epstein Barr virus]]]]
* Direct counts using an [[electron microscope]]. A dilute mixture of virus particles and beads of known size are sprayed onto a special sheet and examined under high magnification. The virions are counted and the number extrapolated to estimate the number of virions in the undiluted mixture.
+
Viruses are an established cause of [[malignancy]] in humans and other species.
* [[Viral plaque|Plaque assays]] involve growing a thin layer of host cells onto a culture dish and adding a dilute mixture of virions onto it. The virions will infect and kill the cells they land on, producing holes in the cell layer known as plaques. The number of plaques can be counted and the number of infectious virions is estimated from it. Importantly, unlike other assays, the plaque assay is the only method that can accurately assess the number of infectious virus particles in a preparation of virus. Notably, most viruses exhibit low particle to PFU (plaque forming units) ratios - [[HIV]] is famous for this,; i.e. often hundreds or thousands of defective particles are generated for each one that can actually productively replicate in a permissive cell.
+
The main viruses associated with human cancers are [[human papillomavirus]], [[hepatitis B]] and [[hepatitis C]] virus, [[Epstein-Barr virus]], and [[human T-lymphotropic virus]].
 +
Hepatitis viruses, including [[hepatitis B]] and [[hepatitis C]], can induce a [[Chronic (medical)|chronic]] viral infection that leads to [[Hepatocellular carcinoma|liver cancer]].<ref> {{cite journal
 +
|author=Koike K
 +
|title=Hepatitis C virus contributes to hepatocarcinogenesis by modulating metabolic and intracellular signalling pathways
 +
|journal=J. Gastroenterol. Hepatol.
 +
|volume=22 Suppl 1
 +
|issue=
 +
|pages=S108–11
 +
|year=2007
 +
|pmid=17567457
 +
|doi=10.1111/j.1440-1746.2006.04669.x}}</ref><ref> {{cite journal
 +
|author=Hu J, Ludgate L
 +
|title=HIV-HBV and HIV-HCV coinfection and liver cancer development
 +
|journal=Cancer Treat. Res.
 +
|volume=133
 +
|issue=
 +
|pages=241–52
 +
|year=2007
 +
|pmid=17672044
 +
|doi=}} </ref> Infection by [[human T-lymphotropic virus]] can lead to [[tropical spastic paraparesis]] and [[adult T-cell leukemia]].<ref> {{cite journal
 +
|author=Bellon M, Nicot C
 +
|title=Telomerase: a crucial player in HTLV-I-induced human T-cell leukemia
 +
|journal=Cancer genomics & proteomics
 +
|volume=4
 +
|issue=1
 +
|pages=21–5
 +
|year=2007
 +
|pmid=17726237
 +
|doi=}}</ref> [[Human papillomaviruses]] are an established cause of cancers of [[cervix]], skin, [[anus]], and [[penis]].<ref> {{cite journal
 +
|author=Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S
 +
|title=Human papillomavirus and cervical cancer
 +
|journal=Lancet
 +
|volume=370
 +
|issue=9590
 +
|pages=890–907
 +
|year=2007
 +
|pmid=17826171
 +
|doi=10.1016/S0140-6736(07)61416-0}}</ref> Within the [[Herpesviridae]], [[Kaposi's sarcoma-associated herpesvirus]] causes [[Kaposi's sarcoma]] and body cavity lymphoma, and [[Epstein–Barr virus]] causes [[Burkitt's lymphoma]], [[Hodgkin’s lymphoma]], [[B cell|B]] [[Lymphoproliferative disorders|lymphoproliferative disorder]] and [[nasopharyngeal carcinoma]].<ref> {{cite journal
 +
|author=Klein E, Kis LL, Klein G
 +
|title=Epstein-Barr virus infection in humans: from harmless to life endangering virus-lymphocyte interactions
 +
|journal=Oncogene
 +
|volume=26
 +
|issue=9
 +
|pages=1297–305
 +
|year=2007
 +
|pmid=17322915
 +
|doi=10.1038/sj.onc.1210240}}</ref>
  
Detection and subsequent isolation of new viruses from patients is a specialised laboratory subject. Normally it requires the use of large facilities, expensive equipment, and trained specialists such as technicians, [[molecular biologist]]s, and [[virologist]]s. Often, this effort is undertaken by state and national governments and shared internationally through organizations like the [[World Health Organization]].
+
===Laboratory diagnosis===
 +
[[Image:CPE rounding.jpg|right|thumb|250px|Cells infected with [[Herpes simplex virus]]. The rounding of the cells, their detachment from the cell sheet is the typical cytopathic effect produced by this virus.]]
 +
{{Main|Laboratory diagnosis of virus}}
 +
 
 +
In the diagnostic laboratory, virus infections are confirmed by several methods that include:
 +
*Growth of the virus in a [[cell culture]] from a specimen taken from the patient.
 +
*Detection of virus-specific [[IgM]] antibody (see below) in the blood.
 +
*Detection of virus antigens by [[ELISA]] in tissues and fluids.
 +
*Detection of virus encoded DNA and RNA by [[PCR]].
 +
*Observation of virus particles by [[electron microscopy]].
  
 
=== Prevention and treatment ===
 
=== Prevention and treatment ===
Because viruses use the machinery of a host cell to reproduce and also reside within them, they are difficult to eliminate without killing the host cell. The most effective [[medicine|medical]] approaches to viral diseases so far are [[vaccination]]s to provide resistance to infection, and drugs which treat the symptoms of viral infections. Patients often ask for, and [[General Practitioner|physician]]s often prescribe, [[antibiotic]]s. These are useless against viruses, and their misuse against viral infections is one of the causes of [[antibiotic resistance]] in [[bacterium|bacteria]]. However, in life-threatening situations the prudent course of action is to begin a course of antibiotic treatment while waiting for test results to determine whether the patient's symptoms are caused by a virus or a bacterial infection{{Fact|date=April 2007}}.
+
Because viruses use the machinery of a host cell to reproduce and reside within them, they are difficult to eliminate without killing the host cell. The most effective [[medicine|medical]] approaches to viral diseases so far are [[vaccination]]s to provide resistance to infection, and [[antiviral drugs]] which treat the symptoms of viral infections.
 +
 
 +
===Host immune response===
 +
The body's first line of defense against viruses is the [[innate immune system]]. This comprises cells and other mechanisms that defend the host from infection in a non-specific manner. This means that the cells of the innate system recognize, and respond to, pathogens in a generic way, but unlike the [[adaptive immune system]], it does not confer long-lasting or protective immunity to the host.<ref name=Alberts>{{cite book | last = Alberts| first = Bruce| coauthors = Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walters | title = Molecular Biology of the Cell; Fourth Edition | publisher = Garland Science| date = 2002 | location = New York and London | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=mboc4.TOC&depth=2 | id = ISBN 0-8153-3218-1}}</ref>
 +
 
 +
[[RNA interference]] is an important innate defense against viruses.<ref>Ding SW, Voinnet O. Antiviral immunity directed by small RNAs. Cell. 2007 Aug 10;130(3):413-26.</ref> Many viruses have a replication strategy that involves double-stranded RNA [[dsRNA]]. When such a virus infects a cell, it releases its RNA molecule or molecules, which immediately bind to a protein complex called [[Dicer]] that cuts the RNA into smaller pieces. A biochemical pathway called the RISC complex is activated which degrades the viral [[mRNA]] and the cell survives the infection. Rotaviruses avoid this mechanism by not uncoating fully inside the cell and by releasing newly produced mRNA through pores in the particle's inner capsid. The genomic [[dsRNA]] remains protected inside the core of the virion.<ref name="pmid15579070">{{cite journal
 +
|author=Patton JT, Vasquez-Del Carpio R, Spencer E
 +
|title=Replication and transcription of the rotavirus genome
 +
|journal=Curr. Pharm. Des.
 +
|volume=10
 +
|issue=30
 +
|pages=3769–77
 +
|year=2004
 +
|pmid=15579070
 +
|doi=}}</ref><ref name="pmid15010218">{{cite journal
 +
|author=Jayaram H, Estes MK, Prasad BV
 +
|title=Emerging themes in rotavirus cell entry, genome organization, transcription and replication
 +
|journal=Virus Res.
 +
|volume=101
 +
|issue=1
 +
|pages=67–81
 +
|year=2004
 +
|pmid=15010218
 +
|doi=10.1016/j.virusres.2003.12.007}}</ref>
 +
 
 +
When the [[adaptive immune system]] of a [[vertebrate]] encounters a virus, it produces specific [[antibodies]] which bind to the virus and render it non-infectious. This is called [[humoral immunity]]. Two types of antibodies are important. The first called [[IgM]] is highly effective at neutralizing viruses but is only produced by the cells of the immune system for a few weeks. The second, called, [[IgG]] is produced indefinitely. The presence of IgM in the blood of the host is used to test for acute infection, whereas IgG indicates an infection sometime in the past.<ref>Greer S, Alexander GJ. Viral serology and detection.
 +
Baillieres Clin Gastroenterol. 1995 Dec;9(4):689-721</ref> Both types of antibodies are measured when tests for [[Immunity (medical)|immunity]] are carried out.<ref>Laurence JC. Hepatitis A and B immunizations of individuals infected with humanimmunodeficiency virus.Am J Med. 2005 Oct;118 Suppl 10A:75S-83S.</ref>
 +
 
 +
A second defense of vertebrates against viruses is called [[cell-mediated immunity]] and involves immune cells known as [[T cells]]. The body's cells constantly display short fragments of their proteins on the cell's surface, and if a T cell recognizes a suspicious viral fragment there, the host cell is destroyed by ''T killer'' cells and the virus-specific T-cells proliferate. Cells such as the [[macrophage]] are specialists at this [[antigen presentation]].<ref>Cascalho M, Platt JL. Novel functions of B cells.Crit Rev Immunol. 2007;27(2):141-51.</ref><ref>Khatri M, Sharma JM. Modulation of macrophages by infectious bursal disease virus.Cytogenet Genome Res. 2007;117(1-4):388-93</ref>
 +
 
 +
Not all virus infections produce a protective immune response in this way. HIV evades the immune system by constantly changing the amino acid sequence of the proteins on the surface of the virion. These persistent viruses evade immune control by sequestration, blockade of [[antigen presentation]], [[cytokine]] resistance, evasion of [[natural killer cell]] activities, escape from [[apoptosis]], and [[antigenic shift]].<ref>Hilleman MR. Strategies and mechanisms for host and pathogen survival in acute and persistent viral infections. Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14560-6. Epub 2004 Aug 5.</ref> Other viruses, called "[[neurotropic virus]]es", are disseminated by neural spread where the [[immune system]] may be unable to reach them.
 +
 
 +
The production of [[interferon]] is an important host defense mechanism.<ref>Le Page C, Genin P, Baines MG, Hiscott J. Interferon activation and innate immunity.Rev Immunogenet. 2000;2(3):374-86.</ref>
 +
 
 +
===Vaccines===
 +
{{details|Vaccination}}
 +
[[Vaccination]] is a cheap and effective way of preventing infections by viruses. Vaccines were used to prevent viral infections long before the discovery of the actual viruses. Their use has resulted in a dramatic decline in morbidity (illness) and mortality (death) associated with viral infections such as [[polio]], [[measles]], [[mumps]] and [[rubella]].<ref name="pmid17068034">{{cite journal
 +
|author=Asaria P, MacMahon E
 +
|title=Measles in the United Kingdom: can we eradicate it by 2010?
 +
|journal=BMJ
 +
|volume=333
 +
|issue=7574
 +
|pages=890–5
 +
|year=2006
 +
|pmid=17068034
 +
|doi=10.1136/bmj.38989.445845.7C}}</ref> [[Smallpox]] infections have been eradicated.<ref name="pmid16989262">{{cite journal
 +
|author=Lane JM
 +
|title=Mass vaccination and surveillance/containment in the eradication of smallpox
 +
|journal=Curr. Top. Microbiol. Immunol.
 +
|volume=304
 +
|issue=
 +
|pages=17–29
 +
|year=2006
 +
|pmid=16989262
 +
|doi=}}</ref> Currently vaccines are available to prevent over thirteen viral infections of humans,<ref name="pmid16364754">{{cite journal
 +
|author=Arvin AM, Greenberg HB
 +
|title=New viral vaccines
 +
|journal=Virology
 +
|volume=344
 +
|issue=1
 +
|pages=240–9
 +
|year=2006
 +
|pmid=16364754
 +
|doi=10.1016/j.virol.2005.09.057}}</ref> and more are used to prevent viral infections of animals.<ref name="pmid17892169">{{cite journal
 +
|author=Pastoret PP, Schudel AA, Lombard M
 +
|title=Conclusions--future trends in veterinary vaccinology
 +
|journal=Rev. - Off. Int. Epizoot.
 +
|volume=26
 +
|issue=2
 +
|pages=489–94, 495–501, 503–9
 +
|year=2007
 +
|pmid=17892169
 +
|doi=}}</ref> Vaccines can consist of live-attenuated or killed viruses, or viral proteins ([[antigens]]).<ref name="pmid16494719">{{cite journal
 +
|author=Palese P
 +
|title=Making better influenza virus vaccines?
 +
|journal=Emerging Infect. Dis.
 +
|volume=12
 +
|issue=1
 +
|pages=61–5
 +
|year=2006
 +
|pmid=16494719
 +
|doi=}}</ref> Live vaccines contain weakened forms of the virus that causes the disease. Such viruses are called attenuated. Live vaccines can be dangerous when given to people with a weak immunity, (who are described as [[immunocompromised]]), because in these people, the weakened virus can cause the original disease.<ref name="pmid1090805">{{cite journal
 +
|author=Thomssen R
 +
|title=Live attenuated versus killed virus vaccines
 +
|journal=Monographs in allergy
 +
|volume=9
 +
|issue=
 +
|pages=155–76
 +
|year=1975
 +
|pmid=1090805
 +
|doi=}}</ref> Biotechnology and genetic engineering techniques are used to produce subunit vaccines. These vaccines use only the [[capsid]] proteins of the virus. [[Hepatitis B]] vaccine is an example of this type of vaccine.<ref name="pmid3018891">{{cite journal
 +
|author=McLean AA
 +
|title=Development of vaccines against hepatitis A and hepatitis B
 +
|journal=Rev. Infect. Dis.
 +
|volume=8
 +
|issue=4
 +
|pages=591–8
 +
|year=1986
 +
|pmid=3018891
 +
|doi=}}</ref> Subunit vaccines are safe for [[immunocompromised]] patients because they cannot cause the disease.<ref name="pmid16221073">{{cite journal
 +
|author=Casswall TH, Fischler B
 +
|title=Vaccination of the immunocompromised child
 +
|journal=Expert review of vaccines
 +
|volume=4
 +
|issue=5
 +
|pages=725–38
 +
|year=2005
 +
|pmid=16221073
 +
|doi=10.1586/14760584.4.5.725}}</ref>
 +
The Yellow Fever virus vaccine, a live-attenuated strain called 17D, is arguably the safest and most effective vaccine ever generated.
 +
 
 +
===Antiviral drugs===
 +
{{details|Antiviral drug}}
 +
[[Image:DT chemical structure.png|left|thumb|100px|The true DNA base [[thymidine]]]]
 +
[[Image:Zidovudine.svg|right|thumb|100px|The antiviral drug [[Zidovudine]] - [[AZT]]]]
  
===Potential uses in therapy===
+
Over the past twenty years, the development of [[antiviral drug]]s has increased rapidly. This has been driven by the AIDS epidemic. Antiviral drugs are often [[nucleoside analogues]], (fake DNA building blocks), which viruses incorporate into their genomes during replication. The life-cycle of the virus is then halted because the newly synthesized DNA is inactive. This is because these analogues lack the [[hydroxyl groups]] which along with [[phosphorus]] atoms, link together to form the strong "backbone" of the DNA molecule. This is called DNA [[chain termination]].<ref name="pmid15592828">{{cite journal
[[Virotherapy]] uses viruses as vectors to treat various diseases, as they can specifically target cells and DNA. It shows promise in the treatment of cancer and as a method for gene therapy.{{Fact|date=April 2007}} Eastern European doctors have used [[phage therapy]] as an alternative to antibiotics for some time and interest in this approach is increasing, due to the high level of [[antibiotic resistance]] now found in some pathogenic bacteria.<ref name="pmid16258815">{{cite journal |author=Matsuzaki S, Rashel M, Uchiyama J, ''et al'' |title=Bacteriophage therapy: a revitalized therapy against bacterial infectious diseases |journal=J. Infect. Chemother. |volume=11 |issue=5 |pages=211-9 |year=2005 |pmid=16258815 |doi=10.1007/s10156-005-0408-9}}</ref>
+
|author=Magden J, Kääriäinen L, Ahola T
 +
|title=Inhibitors of virus replication: recent developments and prospects
 +
|journal=Appl. Microbiol. Biotechnol.
 +
|volume=66
 +
|issue=6
 +
|pages=612–21
 +
|year=2005
 +
|pmid=15592828
 +
|doi=10.1007/s00253-004-1783-3}}</ref> Examples of nucleoside analogues are [[aciclovir]] for [[Herpesviridae|Herpes virus]] infections and [[lamivudine]] for [[HIV]] and [[Hepatitis B]] virus infections. [[Aciclovir]] is one of the oldest and most frequently prescribed antiviral drugs.<ref name="pmid6355051">{{cite journal
 +
|author=Mindel A, Sutherland S
 +
|title=Genital herpes - the disease and its treatment including intravenous acyclovir
 +
|journal=J. Antimicrob. Chemother.
 +
|volume=12 Suppl B
 +
|issue=
 +
|pages=51–9
 +
|year=1983
 +
|pmid=6355051
 +
|doi=}}</ref>
 +
[[Image:G chemical structure.png|left|thumb|100px|[[Guanosine]]]][[Image:Aciclovir.svg|right|thumb|100px|The guanosine analogue [[Aciclovir]]]] Other antiviral drugs in use target different stages of the viral life cycle. [[HIV]] is dependent on a proteolytic enzyme called the [[HIV-1 protease]] for it to become fully infectious. There is a class of drugs called [[protease inhibitors]] which have been designed to inactivate the enzyme.
 +
 
 +
[[Hepatitis C]] is caused by an [[RNA]] virus. In 80% of people infected, the disease is [[Chronic (medical)|chronic]], and without treatment, they are [[infected]] and [[infectious]] for the remainder of their lives. However, there is now an effective treatment using the nucleoside analogue drug [[ribavirin]] combined with [[interferon]].<ref>Witthoft T, Moller B, Wiedmann KH, Mauss S, Link R, Lohmeyer J, Lafrenz M,Gelbmann CM, Huppe D, Niederau C, Alshuth U. Safety, tolerability and efficacy of peginterferon alpha-2a and ribavirin in chronic hepatitis C in clinical practice: The German Open Safety Trial. J Viral Hepat. 2007 Nov;14(11):788-96.</ref> The treatment of chronic [[Asymptomatic carrier|carriers]] of the [[Hepatitis B]] virus by using a similar strategy using [[lamivudine]] is being developed.<ref>Rudin D, Shah SM, Kiss A, Wetz RV, Sottile VM. Interferon and lamivudine vs. interferon for hepatitis B e antigen-positive hepatitis B treatment: meta-analysis of randomized controlled trials.Liver Int. 2007 Nov;27(9):1185-93.</ref>
 +
 
 +
===Notable examples===
 +
{{See|Table of clinically important viruses}}
 +
The clinically most notable<ref name=Microbiology354-366> {{cite book |author=Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C.
 +
|title=Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series) |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD
 +
|year=
 +
|pages= |isbn=0-7817-8215-5 |oclc=
 +
|doi=}} Pages 354-366 </ref> virus species belong to the following families:
 +
<div class="references-small" style="-moz-column-count:3; column-count:3;">
 +
*[[Adenoviridae]]
 +
*[[Picornaviridae]]
 +
*[[Herpesviridae]]
 +
*[[Hepadnaviridae]]
 +
*[[Flaviviridae]]
 +
*[[Retroviridae]]
 +
*[[Orthomyxoviridae]]
 +
*[[Paramyxoviridae]]
 +
*[[Papovaviridae]]
 +
*[[Rhabdoviridae]]
 +
*[[Reoviridae]]
 +
*[[Togaviridae]]
 +
</div>
 +
{| class="wikitable"
 +
|-
 +
|+ Comparison table of clinically important virus families and species
 +
|-
 +
! Family
 +
! [[Baltimore classification|Baltimore group]]
 +
! Important species<ref name=Microbiology354-366Unless> Unless else specified in boxes, the ref is: {{cite book |author=Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C.
 +
|title=Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series) |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD
 +
|year=
 +
|pages= |isbn=0-7817-8215-5 |oclc=
 +
|doi=}} Pages 354-366 </ref>
 +
! [[Viral envelope|envelopment]]<ref name=Microbiology354-366Unless/>
 +
! Virion shape<ref name=Microbiology354-366Unless/>
 +
! Replication site<ref name=Microbiology354-366Unless/>
 +
|-
 +
| [[Adenoviridae]]
 +
| [[dsDNA virus|dsDNA]]
 +
| ''adenovirus''
 +
| non-enveloped
 +
| icosahedral
 +
| nucleus
 +
|-
 +
| [[Picornaviridae]]
 +
| [[positive-sense ssRNA virus|+ssRNA]]
 +
| [[coxsackievirus]], [[hepatitis a virus]], [[poliovirus]]
 +
| non-enveloped
 +
| icosahedral
 +
|-
 +
| [[Herpesviridae]]
 +
| [[dsDNA virus|dsDNA]]
 +
| [[epstein-barr virus]], [[Herpes simplex virus|herpes simplex virus, type 1 and 2]], [[human cytomegalovirus]], [[Kaposi's sarcoma-associated herpesvirus|human herpesvirus, type 8]], [[varicella zoster virus]]
 +
| enveloped
 +
|
 +
| nucleus
 +
|-
 +
| [[Hepadnaviridae]]
 +
| [[dsDNA virus|dsDNA]] and [[ssDNA virus|ssDNA]]
 +
| [[hepatitis B virus]]
 +
| enveloped
 +
| icosahedral
 +
| nucleus
 +
|-
 +
| [[Flaviviridae]]
 +
| [[positive-sense ssRNA virus|+ssRNA]]
 +
| [[hepatitis C virus]]
 +
| enveloped
 +
| icosahedral
 +
|-
 +
| [[Retroviridae]]
 +
| [[positive-sense ssRNA virus|+ssRNA]]
 +
| [[human immunodeficiency virus]] (HIV)
 +
| enveloped
 +
|-
 +
| [[Orthomyxoviridae]]
 +
| [[negative-sense ssRNA virus|-ssRNA]]
 +
| [[influenza virus]]
 +
| enveloped
 +
| spherical
 +
| nucleus<ref name=Microbiology315> {{cite book |author=Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C.
 +
|title=Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series) |publisher=Lippincott Williams &amp; Wilkins |location=Hagerstwon, MD
 +
|year=
 +
|pages= |isbn=0-7817-8215-5 |oclc=
 +
|doi=}} Page 315 </ref>
 +
|-
 +
| [[Paramyxoviridae]]
 +
| [[negative-sense ssRNA virus|-ssRNA]]
 +
| [[measles virus]], [[mumps virus]], [[parainfluenza virus]], [[respiratory syncytial virus]]
 +
| enveloped
 +
| spherical
 +
|-
 +
| [[Papovaviridae]]
 +
| [[ssDNA virus|ssDNA]]
 +
| [[papillomavirus]]
 +
| non-enveloped
 +
| icosahedral
 +
|-
 +
| [[Rhabdoviridae]]
 +
| [[negative-sense ssRNA virus|-ssRNA]]
 +
| [[rabies virus]]
 +
| enveloped
 +
| helical, bullet shaped
 +
|-
 +
| [[Reoviridae]]
 +
| [[double-stranded RNA|dsRNA]]
 +
| [[Rotavirus]]
 +
| non-enveloped
 +
| icosahedral
 +
| cytoplasm
 +
|-
 +
| [[Togaviridae]]
 +
| [[positive-sense ssRNA virus|+ssRNA]]
 +
| [[Rubella virus]]
 +
| enveloped
 +
| icosahedral
 +
|-
 +
|}
  
 
==Applications==
 
==Applications==
[[Image:Polio EM PHIL 1875 lores.PNG|thumb|170px|right|[[Transmission electron microscopy|TEM]] [[micrograph]] of [[Poliovirus]] virions.]]
+
===Life sciences and medicine===
===Life sciences===
+
Viruses are important to the study of [[molecular biology|molecular]] and [[cellular biology]] as they provide simple systems that can be used to manipulate and investigate the functions of cells. The study and use of viruses have provided valuable information about aspects of cell biology. For example, viruses have been useful in the study of [[genetics]] and helped our understanding of the basic mechanisms of [[molecular genetics]], such as [[DNA replication]], [[transcription (genetics)|transcription]], [[RNA processing]], [[translation (genetics)|translation]], [[protein]] transport, and [[immunology]].
Viruses are important to the study of [[molecular biology|molecular]] and [[cellular biology]] as they provide simple systems that can be used to manipulate and investigate the functions of cells. The study and use of viruses have provided valuable information about many aspects of cell biology. For example, viruses have simplified the study of [[genetics]] and helped human understanding of the basic mechanisms of [[molecular genetics]], such as [[DNA replication]], [[transcription (genetics)|transcription]], [[RNA processing]], [[translation (genetics)|translation]], [[protein]] transport, and [[immunology]].
+
 
 +
[[Image:Gene therapy.jpg|right|thumb|250px|[[Gene therapy]] using an [[Adenovirus]] vector]]
 +
 
 +
[[genetics|Geneticists]] often use viruses as [[vector (biology)|vectors]] to introduce genes into cells that they are studying. This is useful for making the cell produce a foreign substance, or to study the effect of introducing a new gene into the genome. In similar fashion, [[virotherapy]] uses viruses as vectors to treat various diseases, as they can specifically target cells and DNA. It shows promising use in the treatment of cancer and in [[gene therapy]]. Eastern European scientists have used [[phage therapy]] as an alternative to antibiotics for some time, and interest in this approach is increasing, due to the high level of [[antibiotic resistance]] now found in some pathogenic bacteria.<ref name="pmid16258815">{{cite journal
 +
|author=Matsuzaki S, Rashel M, Uchiyama J, ''et al''
 +
|title=Bacteriophage therapy: a revitalized therapy against bacterial infectious diseases
 +
|journal=J. Infect. Chemother.
 +
|volume=11
 +
|issue=5
 +
|pages=211-9
 +
|year=2005
 +
|pmid=16258815
 +
|doi=10.1007/s10156-005-0408-9}}</ref>
  
[[genetics|Geneticists]] regularly use viruses as [[vector (biology)|vectors]] to introduce genes into cells that they are studying. This is useful for making the cell produce a foreign substance, or to study the effect of introducing a new gene into the genome. In similar fashion, [[virotherapy]] uses viruses as vectors to treat various diseases, as they can specifically target cells and DNA. It shows promising use in the treatment of cancer and in [[gene therapy]].
+
Granulosis (GV) and nucleo-polyhedrosis viruses (NPV) may also be used as [[biological insecticides]] (''e.g''. [[Cydia pomonella granulosis virus|''Cydia pomonella'' granulovirus]]).
  
 
===Materials science and nanotechnology===
 
===Materials science and nanotechnology===
Current trends in nanotechnology promise to make much more versatile use of viruses. From the viewpoint of a materials scientist, viruses can be regarded as organic nanoparticles{{Fact|date=April 2007}}. Their surface carries specific tools designed to cross the barriers of their host cells. The size and shape of viruses, and the number and nature of the functional groups on their surface, is precisely defined. As such, viruses are commonly used in materials science as scaffolds for covalently linked surface modifications. A particular quality of viruses is that they can be tailored by directed evolution. The powerful techniques developed by life sciences are becoming the basis of engineering approaches towards nanomaterials, opening a wide range of applications far beyond biology and medicine.<ref name=fischlechner >{{cite journal |author=Fischlechner M, Donath E |title=Viruses as Building Blocks for Materials and Devices |url=http://dx.doi.org/doi:10.1002/anie.200603445 |journal=Angewandte Chemie International Edition |volume= |issue= |pages= |year=2007 |doi=10.1002/anie.200603445}}</ref>
+
Current trends in nanotechnology promise to make much more versatile use of viruses. From the viewpoint of a materials scientist, viruses can be regarded as organic nanoparticles.<ref> Proceedings of SPIE -- Volume 6413Smart Materials IV, Nicolas H. Voelcker, Editor, 64130F (Dec. 22, 2006). Hybrid organic-inorganic nanoparticles: controlled incorporation of gold nanoparticles into virus-like particles and application in surface-enhanced Raman spectroscopy
 
+
Marcus Niebert, James Riches, Mark Howes, Charles Ferguson, Robert G. Parton, Anton P. J. Middelberg, Llew Rintoul, and Peter M. Fredericks.Queensland Univ. of Technology (Australia)
In April 2006 scientists at the [[Massachusetts Institute of Technology]] (MIT) created [[nanotechnology|nanoscale]] metallic wires using a [[Genetic engineering|genetically-modified]] virus.<ref name="mitvirusbattery">{{Cite web|url=http://web.mit.edu/newsoffice/2006/virus-battery.html|title=Researchers build tiny batteries with viruses|accessdate=2007-04-05|publisher=MIT News Office}}</ref> The MIT team was able to use the virus to create a working [[Battery (electricity)|battery]] with an [[energy density]] up to three times more than current materials. The potential exists for this technology to be used in [[liquid crystal]]s, [[solar cell]]s, [[fuel cells]], and other electronics in the future.
+
(published online Dec. 22, 2006)</ref>
 +
Their surface carries specific tools designed to cross the barriers of their host cells. The size and shape of viruses, and the number and nature of the functional groups on their surface, is precisely defined. As such, viruses are commonly used in materials science as scaffolds for covalently linked surface modifications. A particular quality of viruses is that they can be tailored by directed evolution. The powerful techniques developed by life sciences are becoming the basis of engineering approaches towards nanomaterials, opening a wide range of applications far beyond biology and medicine.<ref name=fischlechner>{{cite journal
 +
|author=Fischlechner M, Donath E
 +
|title=Viruses as Building Blocks for Materials and Devices
 +
|url=http://dx.doi.org/doi:10.1002/anie.200603445
 +
|journal=Angewandte Chemie International Edition
 +
|volume=
 +
|issue=
 +
|pages=
 +
|year=2007
 +
|doi=10.1002/anie.200603445}}</ref>
  
[[Image:Reconstructed Spanish Flu Virus.jpg|thumb|200px|right|The reconstructed [[1918 influenza]] virus]]
+
Because of their size, shape, and well-defined chemical structures, viruses have been used as templates for organizing materials on the nanoscale. Recent examples include work at the [[Naval Research Laboratory]] in Washington, DC, using Cowpea Mosaic Virus ([[CPMV]]) particles to amplify signals in [[microarray]] based sensors. In this application, the virus particles separate the [[fluorescence|fluorescent]] [[dye]]s used for signaling in order to prevent the formation of non-fluorescent [[dimer]]s that act as quenchers.<ref>''Fluorescent signal amplification of carbocyanine dyes using engineered viral nanoparticles.'' Carissa M. Soto, Amy Szuchmacher Blum, Nikolai Lebedev, Gary J. Vora, Carolyn E. Meador, Angela P. Won, Anju Chatterji, John E. Johnson, and Banahalli R. Ratna, ''Journal of the American Chemical Society'', '''128''', 5184 (2006). </ref> Another example is the use of CPMV as a nanoscale breadboard for molecular electronics.<ref>An Engineered Virus as a Scaffold for Three-Dimensional Self-Assembly on the Nanoscale. Amy Szuchmacher Blum, Carissa M. Soto, Charmaine D. Wilson, Tina L. Brower, Steven K. Pollack, Terence L. Schull, Anju Chatterji, Tianwei Lin, John E. Johnson, Christian Amsinck, Paul Franzon, Ranganathan Shashidhar and Banahalli Ratna, ''Small'', '''7,''' 702 (2005).</ref> In April 2006, scientists at the Massachusetts Institute of Technology (MIT) created nanoscale metallic wires using a [[Genetic engineering|genetically-modified]] virus.<ref name="mitvirusbattery">{{Cite web
 +
|url=http://web.mit.edu/newsoffice/2006/virus-battery.html
 +
|title=Researchers build tiny batteries with viruses|accessdate=2007-04-05|publisher=MIT News Office}}</ref> The MIT team was able to use the virus to create a working battery with an energy density up to three times more than current materials. The potential exists for this technology to be used in [[liquid crystal]]s, solar cells, [[fuel cells]], and other electronics in the future.
  
 
===Weapons===
 
===Weapons===
 
{{details|Biological warfare}}
 
{{details|Biological warfare}}
The ability of viruses to cause devastating [[epidemic]]s in human societies has led to the concern that viruses could be weaponized for [[biological warfare]]. Further concern was raised by the successful recreation of the infamous 1918 influenza virus in a laboratory.<ref name="cdcnews">{{Cite web|url=http://www.cdc.gov/OD/OC/MEDIA/pressrel/r051005.htm|title=Researchers Reconstruct 1918 Pandemic Influenza Virus; Effort Designed to Advance Preparedness|accessdate=2007-04-05|publisher=Centers for Disease Control}}</ref> The [[smallpox]] virus devastated numerous societies throughout history before its eradication. It currently exists in several secure laboratories in the world, and fears that it may be used as a weapon are not totally unfounded. The modern global human population has almost no established resistance to smallpox; if it were to be released, a massive loss of life could be sustained before the virus is brought under control.
+
The ability of viruses to cause devastating [[epidemic]]s in human societies has led to the concern that viruses could be weaponized for [[biological warfare]]. Further concern was raised by the successful recreation of the infamous 1918 influenza virus in a laboratory.<ref name="cdcnews">{{Cite web
 +
|url=http://www.cdc.gov/OD/OC/MEDIA/pressrel/r051005.htm
 +
|title=Researchers Reconstruct 1918 Pandemic Influenza Virus; Effort Designed to Advance Preparedness|accessdate=2007-04-05|publisher=Centers for Disease Control}}</ref> The [[smallpox]] virus devastated numerous societies throughout history before its eradication. It currently exists in several secure laboratories in the world, and fears that it may be used as a weapon are not totally unfounded. The vaccine for smallpox is not safe, and during the years before the eradication of smallpox disease more people became seriously ill as a result of vaccination than did people from smallpox<ref name="pmid12911836">{{cite journal
 +
|author=Aragón TJ, Ulrich S, Fernyak S, Rutherford GW
 +
|title=Risks of serious complications and death from smallpox vaccination: a systematic review of the United States experience, 1963-1968
 +
|journal=BMC public health
 +
|volume=3
 +
|issue=
 +
|pages=26
 +
|year=2003
 +
|pmid=12911836
 +
|doi=10.1186/1471-2458-3-26}}</ref> and smallpox vaccination is no longer universally practiced.<ref name="pmid15578369">{{cite journal
 +
|author=Weiss MM, Weiss PD, Mathisen G, Guze P
 +
|title=Rethinking smallpox
 +
|journal=Clin. Infect. Dis.
 +
|volume=39
 +
|issue=11
 +
|pages=1668–73
 +
|year=2004
 +
|pmid=15578369
 +
|doi=10.1086/425745}}</ref> Thus, the modern global human population has almost no established resistance to smallpox; if it were to be released, a massive loss of life could be sustained before the virus is brought under control.
  
== Etymology ==
+
==Electron micrographs of viruses==
The word is from the [[Latin]] ''virus'' referring to [[poison]] and other noxious substances, first used in English in 1392.<ref name=Etymology_Dictionary>{{cite web | title = virus | work = The Online Etymology Dictionary | url = http://www.etymonline.com/index.php?term=virus | accessdate = 2007-07-16}}</ref> ''Virulent'', from Latin ''virulentus'' "poisonous" dates to 1400.<ref name=OED>{{cite web | title = virulent, a. | work = The Oxford English Dictionary - Online | url = http://dictionary.oed.com | accessdate = 2007-07-16}}</ref> A meaning of "agent that causes infectious disease" is first recorded in 1728,<ref name=Etymology_Dictionary /> before the discovery of viruses by the [[Russians|Russian]]-[[Ukrainians|Ukrainian]] [[biologist]] [[Dmitry Ivanovsky]] in 1892. The adjective ''viral'' dates to 1948.<ref name=OED2>{{cite web | title = viral, a. | work = The Oxford English Dictionary - Online | url = http://dictionary.oed.com | accessdate = 2007-07-16}}</ref> Today, ''virus''  is used to describe the biological viruses discussed above and also as a [[metaphor]] for other parasitically-reproducing things, such as [[meme]]s or [[computer virus]]es (since 1972).<ref name=OED /> The [[neologism]] '''virion''' or viron is used to refer to a single infective viral particle.
+
<gallery>
 +
Image:Norwalk.jpg|[[Norovirus]]. This RNA virus causes winter vomiting disease. It is often in the news as a cause of gastro-enteritis on cruise ships and in hospitals.
 +
 
 +
Image:Caliciviruses2.jpg|Caliciviruses are related to Noroviruses.
 +
 
 +
Image:Human Torovirus.jpg|Torovirus. An enveloped RNA virus.
 +
 
 +
Image:Coronaviruses 004 lores.jpg|Coronaviruses are a group of viruses that have a halo, or crown-like (corona) appearance when viewed under a microscope.
 +
 
 +
Image:Ebola virus em.png|Ebola Virus is a filamentous RNA virus.
 +
 
 +
Image:Measles virus.JPG|[[Measles]] virus. This is called a ''thin section'' where the virus particle has been cut in two.
 +
 
 +
Image:Respiratory syncytial virus 01.jpg|[[Respiratory Syncytial Virus]] (RSV). In this preparation the ribonucleoprotein can be seen as a herring bone pattern.
 +
 
 +
Image:Parvovirus in Blood.jpg|[[Parvovirus B19]]. Parvovirus B19 is a small DNA virus best known for causing a childhood exanthema called fifth disease or erythema infectiosum.
 +
 
 +
Image:Papilloma Virus (HPV) EM.jpg|[[Human Papilloma Virus]]
  
The Latin word is from a [[Proto-Indo-European language|Proto-Indo-European]] root *{{PIE|weis-}} "to melt away, to flow," used of foul or malodorous fluids. It is a cognate of [[Sanskrit]] ''{{IAST|viṣh}}'' "poison", [[Avestan]] ''viš-'' "poison", Greek  ''ios'' "poison", [[Old Church Slavonic]]  ''višnja'' "cherry", [[Old Irish]] ''fi'' "poison", [[Welsh language|Welsh]] ''gwy'' "fluid"; Latin ''viscum'' (see [[viscous]]) "sticky substance" is also from the same root.
+
Image:EM of influenza virus.jpg|[[Influenza virus]]
  
The English plural form of ''virus'' is ''viruses''. No reputable dictionary gives any other form, including such "reconstructed" Latin plural forms as ''viri'' (which actually means ''men''), and no plural form appears in the Latin corpus (See [[plural of virus]]). ''Virus'' does not have a traditional Latin plural because its original sense, ''poison'' is a [[mass noun]] like the English word ''furniture'', and, as pointed out above, English use of ''virus'' to denote the agent of a disease predates the discovery that these agents are microscopic parasites and thus in principle countable.
+
Image:Herpes simplex virus TEM B82-0474 lores.jpg|Transmission electron micrograph of [[Herpes]] virus an enveloped virus that looks like fried eggs by negative stain electron microscopy.
  
== Philosophy ==
+
Image:Polio EM PHIL 1875 lores.PNG|[[Transmission electron microscopy|TEM]] [[micrograph]] of [[Poliovirus]] virions.
  
Viruses have attracted attention of philosophers and critics because of their position at the margins of life and their unique method of propagation. [[Susan Sontag]] argues that viruses have been used detrimentally as metaphors for social phenomena.<ref>[[Susan Sontag|Sontag, Susan]] (1978). [[Illness as Metaphor]]. Farrar Straus & Giroux.</ref> [[Gilles Deleuze]] and [[Félix Guattari]] use the virus as an example of [[Rhizome (philosophy)|rhizomatic]] being because of its nomadic movement through host organisms. They note that viruses can be responsible for [[Horizontal gene transfer|"aparallel evolution"]], which they see as disruptive to arborescent phylogentic trees. <ref>[[Gilles Deleuze|Deleuze, Gilles]] and [[Félix Guattari]] (1987) [1980]. ''[[A Thousand Plateaus]]''. University of Minnesota Press.</ref>
+
</gallery>
  
 
==See also==
 
==See also==
{{Wikibookspar||Viruses, Prions, and Viroids (General Biology)|}}
+
*[[Influenza]]
{{Commons|Category:Viruses|Virus}}
+
*[[Rotavirus]]
{{Wiktionary}}
+
*[[Herpes simplex virus]]
{{Wikispecies}}
+
*[[Hepatitis B virus]]
*[[List of viruses]]
+
*[[Satellite (biology)|Satellite]]
*[[Nanobes]]
+
* [[Neurotropic virus]]
*[[Nanobacteria]]
+
*[[Bacteriophages]] (bacterial viruses)
*[[Provirus]]
 
*[[Transduction]]
 
*[[Bioaerosol]]
 
*[[Oncolytic virus]]
 
*[[Animal virology|Animal viruses]] <br clear="all" />
 
  
==Footnotes==
 
<!-- ---------------------------------------------------------------
 
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discussion of different citation methods and how to generate
 
footnotes using the <ref> & </ref> tags and the {{Reflist}} template
 
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{{Reflist|2}}
 
  
 
==References==
 
==References==
<div class="references-small" style="-moz-column-count:2; column-count:2;">
+
{{Reflist|2}}
* [http://viperdb.scripps.edu/ Icosahedral virus structure]
 
* Villarreal, Luis P. (2005). "Viruses and the Evolution of Life." Washington, ASM Press.
 
* [http://www.virology.net/ All the Virology on the WWW]
 
* [http://www-micro.msb.le.ac.uk/109/structure.html University of Leicester online notes] - Virus Structure
 
* [http://www.plazamedicine.com/index.html Chronic Active Human Herpesvirus-6 (HHV-6) Infection: A New Disease Paradigm]
 
* Gelderblom, Hans R. (1996).  [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.chapter.2252 41. Structure and Classification of Viruses] in ''[http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed Medical Microbiology] 4th ed.'' Samuel Baron ed. The University of Texas Medical Branch at Galveston. ISBN 0-9631172-1-1
 
* Radetsky, Peter (1994). ''The Invisible Invaders: Viruses and the Scientists Who Pursue Them.'' Backbay Books, ISBNs 0316732168 (hc), 0316732176 (pb).
 
* Theiler, Max and Downs, W. G. (1973). ''The Arthropod-Borne Viruses of Vertebrates: An Account of the Rockefeller Foundation Virus Program 1951-1970''. Yale University Press.
 
* {{NCBI-scienceprimer}}</div>
 
  
==External links==
+
{{Viruses}}
*[http://www.duesberg.com HIV] - HIV/AIDS Research
 
*[http://www.vrc.nih.gov Vaccine Research Center (VRC)] - Information concerning vaccine research studies
 
*[http://www.home-air-purifier-expert.com/bioaerosols.html Chart of viral pathogens which contribute to indoor air pollution]
 
*[http://www.isracast.com/tech_news/260106_tech.aspx Viruses: The new cancer hunters] - An IsraCast article on virotherapy
 
*[http://www.virology.net/Big_Virology/BVHomePage.html The Big Picture Book of Viruses] - Pictures and general information on many viruses
 
*[http://www.sciam.com/article.cfm?chanID=sa006&articleID=00023290-03BC-1F5D-905980A84189EEDF Scientific American Magazine (October 2003 Issue) Tumor-Busting Viruses]
 
* [http://www.vbrc.org Detailed genomic and bioinformatic information about Category A, B, and C priority pathogens at NIH-funded database].
 
* [http://www.larger-than-life.org/modules.php?name=Content&pa=showpage&pid=8 Assorted information about Viruses]
 
* [http://www.cosmosmagazine.com/node/1024 "A few good viruses"], a feature story on how viruses are being 'hijacked' for the benefit of humanity. [[Cosmos Magazine|''Cosmos Magazine'']], by Hamish Clarke, 7 February 2007
 
  
[[Category:English words and phrases of foreign origin]]
+
[[Category:primary care]]
[[Category:Latin words and phrases]]
 
 
[[Category:Virology|*]]
 
[[Category:Virology|*]]
[[Category:Viruses| ]]
+
[[Category:Viruses|Viruses]]
 +
[[Category:Microbiology]]
  
 
{{Link FA|ja}}
 
{{Link FA|ja}}
 
 
[[af:Virus]]
 
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[[als:Virus (Medizin)]]
 
[[als:Virus (Medizin)]]
 
[[ar:فيروس]]
 
[[ar:فيروس]]
 
[[zh-min-nan:Pēⁿ-to̍k]]
 
[[zh-min-nan:Pēⁿ-to̍k]]
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[[tr:Virüs]]
 
[[uk:Вірус]]
 
[[uk:Вірус]]
[[ur:وائرس]]
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[[ur:حُمہ]]
[[yi:וויירוס]]
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[[yi:ווירוס]]
 
[[zh:病毒]]
 
[[zh:病毒]]
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Latest revision as of 02:00, 6 February 2013

Viruses
Rotavirus
Rotavirus
Virus classification
Group: I–VII
Groups

I: dsDNA viruses
II: ssDNA viruses
III: dsRNA viruses
IV: (+)ssRNA viruses
V: (-)ssRNA viruses
VI: ssRNA-RT viruses
VII: dsDNA-RT viruses

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Experimental / Informatics

List of terms related to Virus

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]



A virus (from the Latin virus meaning "toxin" or "poison"), is a sub-microscopic infectious agent that is unable to grow or reproduce outside a host cell. Each viral particle, or virion, consists of genetic material, DNA or RNA, within a protective protein coat called a capsid. The capsid shape varies from simple helical and icosahedral (polyhedral or near-spherical) forms, to more complex structures with tails or an envelope. Viruses infect cellular life forms and are grouped into animal, plant and bacterial types, according to the type of host infected.

Biologists debate whether or not viruses are living organisms. Some consider them non-living as they do not meet the criteria of the definition of life. For example, unlike most organisms, viruses do not have cells. However, viruses have genes and evolve by natural selection. Others have described them as organisms at the edge of life. Viral infections in human and animal hosts usually result in an immune response and disease. Often, a virus is completely eliminated by the immune system. Antibiotics have no effect on viruses, but antiviral drugs have been developed to treat life-threatening infections. Vaccines that produce lifelong immunity can prevent viral infections.

Etymology

The word is from the Latin virus referring to poison and other noxious substances, first used in English in 1392.[1] Virulent, from Latin virulentus, "poisonous", dates to 1400.[2] A meaning of "agent that causes infectious disease" is first recorded in 1728,[1] before the discovery of viruses by the Russian-Ukrainian biologist Dmitry Ivanovsky in 1892. The adjective viral dates to 1948.[3] Today, virus is used to describe the biological viruses discussed above and as a metaphor for other parasitically-reproducing things, such as memes or computer viruses (since 1972).[2] The term virion is also used to refer to a single infective viral particle. The English plural form of virus is viruses.

Discovery of viruses

Viral diseases such as rabies, yellow fever and smallpox have affected humans for centuries. There is hieroglyphical evidence of polio in ancient Egyptian medicine,[4] though the cause of this disease was unknown at the time. In the 10th century, Muhammad ibn Zakarīya Rāzi (Rhazes) wrote the Treatise on Smallpox and Measles, in which he gave the first clear descriptions of smallpox and measles.[5] In the 1020s, Avicenna wrote The Canon of Medicine, in which he discovered the contagious nature of infectious diseases, such as tuberculosis and sexually transmitted diseases, and their distribution through bodily contact or through water and soil;[6] stated that bodily secretion is contaminated by "foul foreign earthly bodies" before being infected;[7] and introduced the method of quarantine as a means of limiting the spread of contagious disease.[8]

When the Black Death bubonic plague reached al-Andalus in the 14th century, Ibn Khatima discovered that infectious diseases are caused by microorganisms which enter the human body. The etiologic cause of the bubonic plague would later be identified as a bacterium. Another 14th century Andalusian physician, Ibn al-Khatib (1313-1374), wrote a treatise called On the Plague, in which he stated how infectious diseases can be transmitted through bodily contact and "through garments, vessels and earrings."[7] In 1717, Mary Montagu, the wife of an English ambassador to the Ottoman Empire, observed local women inoculating their children against smallpox.[9] In the late 18th century, Edward Jenner observed and studied Miss Sarah Nelmes, a milkmaid who had previously caught cowpox and was found to be immune to smallpox, a similar, but devastating virus. Jenner developed the smallpox vaccine based on these findings. After lengthy vaccination campaigns, the World Health Organization (WHO) certified the eradication of smallpox in 1979.

In the late 19th century, Charles Chamberland developed a porcelain filter with pores small enough to remove cultured bacteria from their culture medium.[10] Dimitri Ivanovski used this filter to study an infection of tobacco plants, now known as tobacco mosaic virus. He passed crushed leaf extracts of infected tobacco plants through the filter, then used the filtered extracts to infect other plants, thereby proving that the infectious agent was not a bacterium. Similar experiments were performed by several other researchers, with similar results. These experiments showed that viruses are orders of magnitude smaller than bacteria. The term virus was coined by the Dutch microbiologist Martinus Beijerinck, who showed, using methods based on the work of Ivanovski, that tobacco mosaic disease is caused by something smaller than a bacterium. He coined the Latin phrase "contagium vivum fluidum" (which means "soluble living germ") as the first idea of the virus.[11] The first human virus identified was Yellow Fever virus.

In the early 20th century, Frederick Twort discovered that bacteria could be infected by viruses.[12] Felix d'Herelle, working independently, showed that a preparation of viruses caused areas of cellular death on thin cell cultures spread on agar. Counting the dead areas allowed him to estimate the original number of viruses in the suspension. The invention of electron microscopy provided the first look at viruses. In 1935, Wendell Stanley crystallized the tobacco mosaic virus and found it to be mostly protein.[13] A short time later, the virus was separated into protein and nucleic acid parts.[14][15] In 1939, Max Delbrück and E.L. Ellis demonstrated that, in contrast to cellular organisms, bacteriophage reproduce in "one step", rather than exponentially.[16]

A major problem for early virologists was the inability to propagate viruses on sterile culture media, as is done with cellular microorganisms. This limitation required medical virologists to infect living animals with infectious material, which is dangerous. The first breakthrough came in 1931, when Ernest William Goodpasture demonstrated the growth of influenza and several other viruses in fertile chicken eggs.[17] However, some viruses would not grow in chicken eggs, and a more flexible technique was needed for propagation of viruses. The solution came in 1949 when John Franklin Enders, Thomas H. Weller and Frederick Chapman Robbins together developed a technique to grow the polio virus in cultures of living animal cells.[18] Their methods have since been extended and applied to the growth of viruses and other infectious agents that do not grow on sterile culture media.

Origins

The origin of modern viruses is not entirely clear. It may be that no single mechanism can account for their origin.[19] They do not fossilize well, so molecular techniques have been the most useful means of hypothesising how they arose.[20] Research in microfossil identification and molecular biology may yet discern fossil evidence dating to the Archean or Proterozoic eons. Two main hypotheses currently exist.[21]

Small viruses with only a few genes may be runaway stretches of nucleic acid originating from the genome of a living organism. Their genetic material could have been derived from transferable genetic elements such as plasmids or transposons, that are prone to moving within, leaving, and entering genomes. New viruses are emerging de novo and therefore, it is not always the case that viruses have "ancestors".[22]

Viruses with larger genomes, such as poxviruses, may have once been small cells that parasitized larger host cells. Over time, genes not required by their parasitic lifestyle would have been lost in a streamlining process known as "retrograde-evolution" or "reverse-evolution". The bacteria Rickettsia and Chlamydia are living cells that, like viruses, can only reproduce inside host cells. They lend credence to the streamlining hypothesis, as their parasitic lifestyle is likely to have caused the loss of genes that enabled them to survive outside a host cell.

It is possible that viruses represent a primitive form of self replicating DNA and are a precursor to life as it is currently defined.[23] Other infectious particles which are even simpler in structure than viruses include viroids, satellites, and prions.

Classification

In taxonomy, the classification of viruses is difficult owing to the lack of a fossil record and the dispute over whether they are living or non-living.[24][25] They do not fit easily into any of the domains of biological classification, and classification begins at the family rank. However, the domain name of Acytota (without cells) has been suggested. This would place viruses on a par with the other domains of Eubacteria, Archaea, and Eukarya. Not all families are currently classified into orders, nor all genera classified into families.

In 1962, André Lwoff, Robert Horne, and Paul Tournier were the first to develop a means of virus classification, based on the Linnaean hierarchical system.[26] This system based classification on phylum, class, order, family, genus, and species. Viruses were grouped according to their shared properties (not of their hosts) and the type of nucleic acid forming their genomes.[27] Following this initial system, a few modifications were made and the International Committee on Taxonomy of Viruses was developed (ICTV).

ICTV classification

The International Committee on Taxonomy of Viruses (ICTV) developed the current classification system and put in place guidelines that put a greater weighting on certain virus properties to maintain family uniformity. A universal system for classifying viruses, and a unified taxonomy, has been established since 1966. In determining order, taxonomists should consider the type of nucleic acid present, whether the nucleic acid is single- or double-stranded, and the presence or absence of an envelope. After these three main properties, other characteristics can be considered: the type of host, the capsid shape, immunological properties and the type of disease it causes. The system makes use of a series of ranked taxons. The general structure is as follows:

Order (-virales)
Family (-viridae)
Subfamily (-virinae)
Genus (-virus)
Species (-virus)

The recognition of orders is very recent; to date, only three have been named, and most families remain unplaced. The committee does not formally distinguish between subspecies, strains, and isolates. In total there are three orders, 56 families, nine subfamilies, and 233 genera. ICTV recognizes about 1,550 virus species, but about 30,000 virus strains and isolates are being tracked by virologists.[28]

The Nobel Prize-winning biologist David Baltimore devised the Baltimore classification system.[29][30] The ICTV classification system is used in conjunction with the Baltimore classification system in modern virus classification.[31][32][33]

Baltimore Classification

The Baltimore Classification of viruses is based on the method of viral mRNA synthesis.

The Baltimore classification of viruses is based on the mechanism of mRNA production. Viruses must generate positive strand mRNAs from their genomes to produce proteins and replicate themselves, but different mechanisms are used to achieve this in each virus family. This classification places viruses into seven groups:

As an example of viral classification, the chicken pox virus, Varicella zoster (VZV), belongs to family Herpesviridae, subfamily Alphaherpesvirinae and genus Varicellovirus. It remains unranked in terms of order. VZV is in Group I of the Baltimore Classification because it is a dsDNA virus that does not use reverse transcriptase.

Structure

A complete virus particle, known as a virion, consists of nucleic acid surrounded by a protective coat of protein called a capsid. Viruses can have a lipid "envelope" derived from the host cell membrane. A capsid is made from proteins encoded by the viral genome and its shape serves as the basis for morphological and antigenic distinction.[34][35] Virally coded protein subunits will self-assemble to form a capsid, generally requiring the presence of the virus genome. However, complex viruses code for proteins which assist in the construction of their capsid.[21] Proteins associated with nucleic acid are known as nucleoproteins, and the association of viral capsid proteins with viral nucleic acid is called a nucleocapsid.

In general, there are four main morphological virus types:

Helical viruses
Diagram of a helical capsid
Helical capsids are composed of a single type of subunit stacked around a central axis to form a helical structure which may have a central cavity, or hollow tube. This arrangement results in rod-shaped or filamentous virions: these can be anything from short and highly rigid, to long and very flexible. The genetic material, generally single-stranded RNA, but ssDNA in some cases, is bound into the protein helix, by interactions between the negatively-charged nucleic acid and positive charges on the protein. Overall, the length of a helical capsid is related to the length of the nucleic acid contained within it and the diameter is dependent on the size and arrangement of protomers. The well-studied Tobacco mosaic virus is an example of a helical virus.
Icosahedral viruses
Electron micrograph of icosahedral virions
Icosahedral capsid symmetry results in a spherical appearance of viruses at low magnification but actually consists of capsomers arranged in a regular geometrical pattern, similar to a soccer ball, hence they are not truly "spherical". Capsomers are ring shaped constructed from five to six copies of protomers. These associate via non-covalent bonding to enclose the viral nucleic acid, though generally less intimately than helical capsids, and may involve one or more protomers.

Icosahedral architecture was employed by R. Buckminster Fuller in his geodesic dome, and is the most efficient way of creating an enclosed robust structure from multiple copies of a single protein. The number of proteins required to form a spherical virus capsid is denoted by the T-number,[36] where 60×t proteins are necessary. In the case of the hepatitis B virus the T-number is 4, and 240 proteins assemble to form the capsid.

Enveloped viruses
Herpes zoster virus
Viruses are able to envelope themselves in a modified form of one of the cell membranes either the outer membrane surrounding an infected host cell, or from internal membranes such as nuclear membrane or endoplasmic reticulum, thus gaining an outer lipid bilayer known as a viral envelope. This membrane is studded with proteins coded for by the viral genome and host genome; however the lipid membrane itself and any carbohydrates present are entirely host-coded. The Influenza virus and HIV use this strategy.

The viral envelope can give a virion a few distinct advantages over other capsid-only virions, such as protection from enzymes and certain chemicals. The proteins in it can include glycoproteins functioning as receptor molecules, allowing host cells to recognize and bind these virions, resulting in the possible uptake of the virion into the cell. Most enveloped viruses are dependent on the envelope for infectivity.

Complex viruses
Diagram of a bacteriophage
These viruses possess a capsid which is neither purely helical, nor purely icosahedral, and which may possess extra structures such as protein tails or a complex outer wall. Some bacteriophages have a complex structure consisting of an icosahedral head bound to a helical tail, the latter of which may have a hexagonal base plate with protruding protein tail fibres.
Poxvirus
The Poxviruses are large, complex viruses which have an unusual morphology. The viral genome is associated with proteins within a central disk structure known as a nucleoid. The nucleoid is surrounded by a membrane and two lateral bodies of unknown function. The virus has an outer envelope with a thick layer of protein studded over its surface. The whole particle is slightly pleiomorphic, ranging from ovoid to brick shape.[37]

Electron microscopy

File:Relative scale.svg Electron microscopy is the most common method used to study the morphology of viruses. To increase the contrast between viruses and the background, electron-dense "stains" are used. These are solutions of salts of heavy metals such as tungsten, that scatter the electrons from regions covered with the stain. When virus particles are coated with stain (positive staining), fine detail is obscured. Negative staining overcomes this problem by staining the background only.[38]

Size

A medium-sized virion next to a flea is roughly equivalent to a human next to a mountain twice the size of Mount Everest. Some filoviruses have a total length of up to 1400 nm, however their capsid diameters are only about 80 nm. Most viruses which have been studied have a capsid diameter between 10 and 300 nanometres. Most viruses are unable to be seen with a light microscope but some are as large or larger than the smallest bacteria and can be seen under high optical magnification. More commonly, both scanning and transmission electron microscopes are used to visualize virus particles.

Genome

Genomic diversity among viruses
Property Parameters
Nucleic acid
  • DNA
  • RNA
  • Both DNA and RNA
Shape
  • Linear
  • Circular
  • Segmented
Strandedness
  • Single-stranded
  • Double-stranded
  • Double-stranded with regions of single-strandedness
Sense
  • Positive sense (+)
  • Negative sense (-)
  • Ambisense (+/-)

An enormous variety of genomic structures can be seen among viral species; as a group they contain more structural genomic diversity than the entire kingdoms of either plants, animals, or bacteria.[39]

Nucleic acid

A virus may employ either DNA or RNA as the nucleic acid. Rarely do they contain both, however cytomegalovirus is an exception to this, possessing a DNA core with several mRNA segments.[21] By far most viruses have RNA. Plant viruses tend to have single-stranded RNA and bacteriophages tend to have double-stranded DNA.[21] Some virus species possess abnormal nucleotides, such as hydroxymethylcytosine instead of cytosine, as a normal part of their genome.[21]

Shape

Viral genomes may be circular, such as polyomaviruses, or linear, such as adenoviruses. The type of nucleic acid is irrelevant to the shape of the genome. Among RNA viruses, the genome is often divided up into separate parts within the virion and are called segmented. Double-stranded RNA genomes and some single-stranded RNA genomes are segmented.[21] Each segment often codes for one protein and they are usually found together in one capsid. Every segment is not required to be in the same virion for the overall virus to be infectious, as demonstrated by the brome mosaic virus.[21]

Strandedness

A viral genome, irrespective of nucleic acid type, may be either single-stranded or double-stranded. Single-stranded genomes consist of an unpaired nucleic acid, analogous to one-half of a ladder split down the middle. Double-stranded genomes consist of 2 complementary paired nucleic acids, analogous to a ladder. Viruses, such as those belonging to the Hepadnaviridae, contain a genome which is partially double-stranded and partially single-stranded.[39] Viruses that infect humans include double-stranded RNA (e.g. Rotavirus), single-stranded RNA (e.g. Influenza virus), single-stranded DNA (e.g. Parvovirus B19) and double-stranded DNA (Herpes virus).

Sense

For viruses with RNA as their nucleic acid, the strands are said to be either positive-sense (called the plus-strand) or negative-sense (called the minus-strand), depending on whether it is complementary to viral mRNA. Positive-sense viral RNA is identical to viral mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation. DNA nomenclature is similar to RNA nomenclature, in that the coding strand for the viral mRNA is complementary to it (-), and the non-coding strand is a copy of it (+).

Genome size

Genome size in terms of the weight of nucleotides varies between species. The smallest genomes code for only four proteins and weigh about 106 Daltons, the largest weigh about 108 Daltons and code for over one hundred proteins.[21] RNA viruses generally have smaller genome sizes than DNA viruses due to a higher error-rate when replicating, resulting in a maximum upper size limit. Beyond this limit, errors in the genome when replicating render the virus useless or uncompetitive. To compensate for this, RNA viruses often have segmented genomes where the genome is split into smaller molecules, thus reducing the chance of error.[40] In contrast, DNA viruses generally have larger genomes due to the high fidelity of their replication enzymes.[39]

Gene reassortment

There is an evolutionary advantage in having a segmented genome. Different strains of a virus with a segmented genome, from a pig or a bird or a human for example, such as Influenza virus, can shuffle and combine with other genes producing progeny viruses or (offspring) that have unique characteristics. This is called reassortment or viral sex.[41] This is one reason why Influenza virus constantly changes.[42]

Genetic recombination

Genetic recombination is the process by which a strand of DNA is broken and then joined to the end of a different DNA molecule. This can occur when viruses infect cells simultaneously and studies of viral evolution have shown that recombination has been rampant in the species studied.[43] Recombination is common to both RNA and DNA viruses.[44][45]

Genetic change

Viruses undergo genetic change by several mechanisms. These include a process called genetic drift where individual bases in the DNA or RNA mutate to other bases. Most of these point mutations are silent in that they do not change the protein that the gene encodes, but others can confer evolutionary advantages such as resistance to antiviral drugs.[46] Antigenic shift is where there is a major change in the genome of the virus. This occurs as a result of recombination or reassortment (see above). When this happens with influenza viruses, pandemics may result.[47][48] By genome rearrangement the structure of the gene changes although no mutations have necessarily occurred.[49]

RNA viruses are much more likely to mutate than DNA viruses for the reasons outlined above. Viruses often exist as quasispecies or swarms of viruses of the same species but with slightly different genome nucleoside sequences. Such quasispecies are a prime target for natural selection.[50]

Replication

Viral populations do not grow through cell division, because they are acellular; instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves. A virus can still cause degenerative effects within a cell without causing its death; collectively these are termed cytopathic effects.

Virus life cycle

The life cycle of viruses differs greatly between species (see below) but there are six basic stages in the life cycle of viruses: File:Virus Replication.svg

  • Attachment is a specific binding between viral capsid proteins and specific receptors on the host cellular surface. This specificity determines the host range of a virus. For example, the human immunodeficiency virus (HIV) infects only human T cells, because its surface protein, gp120, can interact with CD4 and receptors on the T cell's surface. This mechanism has evolved to favour those viruses that only infect cells that they are capable of replicating in. Attachment to the receptor can induce the viral-envelope protein to undergo changes that results in the fusion of viral and cellular membranes.
  • Penetration: following attachment, viruses enter the host cell through receptor mediated endocytosis or membrane fusion.
  • Uncoating is a process in which the viral capsid is degraded by viral enzymes or host enzymes thus releasing the viral genomic nucleic acid.
  • Replication involves synthesis of viral messenger RNA (mRNA) for viruses except positive sense RNA viruses (see above), viral protein synthesis and assembly of viral proteins and viral genome replication.
  • Following the assembly of the virus particles post-translational modification of the viral proteins often occurs. In viruses such as HIV, this modification, (sometimes called maturation), occurs after the virus has been released from the host cell.[51]
  • Viruses are released from the host cell by lysis (see below). Enveloped viruses (e.g., HIV) typically are released from the host cell by budding. During this process, the virus acquires its phospholipid envelope which contains embedded viral glycoproteins.

DNA viruses

Animal DNA viruses, such as herpesviruses, enter the host via endocytosis, the process by which cells take in material from the external environment. Frequently after a chance collision with an appropriate surface receptor on a cell, the virus penetrates the cell, the viral genome is released from the capsid, and host polymerases begin transcribing viral mRNA. New virions are assembled and released either by cell lysis or by budding off the cell membrane.

RNA viruses

Animal RNA viruses can be placed into about four different groups depending on their modes of replication. The polarity of the RNA largely determines the replicative mechanism, as well as whether the genetic material is single-stranded or double-stranded. Some RNA viruses are actually DNA-based but use an RNA-intermediate to replicate. RNA viruses are dependent on virally encoded RNA replicase to create copies of their genomes.

Reverse transcribing viruses

Reverse transcribing viruses replicate using reverse transcription, which is the formation of DNA from an RNA template. Reverse transcribing viruses containing RNA genomes use a DNA intermediate to replicate, whereas those containing DNA genomes use an RNA intermediate during genome replication. Both types use the reverse transcriptase enzyme to carry out the nucleic acid conversion. Both types are susceptible to antiviral drugs that inhibit the reverse transcriptase enzyme, e.g. zidovudine and lamivudine.

An example of the first type is HIV which is a retrovirus. Retroviruses often integrate the DNA produced by reverse transcription into the host genome. This is why HIV infection can at present, only be treated and not cured.

Examples of the second type are the Hepadnaviridae, which includes the Hepatitis B virus and the Caulimoviridae - e.g. Cauliflower mosaic virus.

Bacteriophages

Transmission electron micrograph of multiple bacteriophages attached to a bacterial cell wall

Bacteriophages infect specific bacteria by binding to surface receptor molecules and then enter the cell. Within a short amount of time, in some cases, just minutes, bacterial polymerase starts translating viral mRNA into protein. These proteins go on to become either new virions within the cell, helper proteins which help assembly of new virions, or proteins involved in cell lysis. Viral enzymes aid in the breakdown of the cell membrane, and in the case of the T4 phage, in just over twenty minutes after injection over three hundred phages could be released.

Lifeform debate

Viruses have been described as "organisms at the edge of life",[52] but argument continues over whether viruses are truly alive. According to the United States Code they are considered microorganisms in the sense of biological weaponry and malicious use. Scientists, however, are divided. Things become more complicated as they look at viroids and prions. Viruses resemble other organisms in that they possess genes and can evolve in infected cells by natural selection.[53][54] They can reproduce by creating multiple copies of themselves through self-assembly.

Viruses do not have a cell structure (regarded as the basic unit of life), although they do have genes. Additionally, although they reproduce, they do not self-metabolize and require a host cell to replicate and synthesize new products. However, bacterial species such as Rickettsia and Chlamydia are considered living organisms but are unable to reproduce outside a host cell.

An argument can be made that accepted forms of life use cell division to reproduce, whereas viruses spontaneously assemble within cells. The comparison is drawn between viral self-assembly and the autonomous growth of non-living crystals. Virus self-assembly within host cells has implications for the study of the origin of life, as it lends credence to the hypothesis that life could have started as self-assembling organic molecules.[55]

If viruses are considered alive, then the criteria specifying life will have to exclude the cell. If viruses are said to be alive, the question could follow of whether even smaller infectious particles, such as viroids and prions, are alive.

Viruses and disease

For more examples of diseases caused by viruses see List of infectious diseases.

Examples of common human diseases caused by viruses include the common cold, the flu, chickenpox and cold sores. Serious diseases such as Ebola, AIDS, avian influenza and SARS are caused by viruses. The relative ability of viruses to cause disease is described in terms of virulence. Other diseases are under investigation as to whether they too have a virus as the causative agent, such as the possible connection between Human Herpesvirus Six (HHV6) and neurological diseases such as multiple sclerosis and chronic fatigue syndrome. There is current controversy over whether the borna virus, previously thought of as causing neurological diseases in horses, could be responsible for psychiatric illnesses in humans.[56]

Viruses have different mechanisms by which they produce disease in an organism, which largely depends on the species. Mechanisms at the cellular level primarily include cell lysis, the breaking open and subsequent death of the cell. In multicellular organisms, if enough cells die the whole organism will start to suffer the effects. Although viruses cause disruption of healthy homeostasis, resulting in disease, they may exist relatively harmlessly within an organism. An example would include the ability of the herpes simplex virus, which cause cold sores, to remain in a dormant state within the human body. This is called latency[57] and is a characteristic of the herpes viruses including the Epstein-Barr virus, which causes glandular fever, and the Varicella zoster virus, which causes chicken pox. Latent chickenpox infections return in later life as the disease called shingles.

Some viruses can cause life-long or chronic infections, where the viruses continue to replicate in the body despite the hosts' defense mechanisms.[58] This is common in Hepatitis B virus and Hepatitis C Virus infections. People chronically infected with the Hepatitis B virus are known as carriers who serve as reservoirs of infectious virus. In some populations, with a high proportion of carriers, the disease is said to be endemic.[59] When diagnosing Hepatitis B virus infections, it is important to distinguish between acute and chronic infections.[60]

Epidemiology

Viral epidemiology is the branch of medical science dealing with the transmission and control of virus infections in humans. Transmission of viruses can be vertical, that is from mother to child, or horizontal, which means from person to person. Examples of vertical transmission include Hepatitis B virus and HIV where the baby is born already infected with the virus.[61] Another, more rare, example is the Varicella zoster virus, which although causing relatively mild infections in humans, can be fatal to the foetus and newly born baby.[62] Horizontal transmission is the most common mechanism of spread of viruses in populations. Transmission can be exchange of blood by sexual activity, e.g. HIV, Hepatitis B and Hepatitis C; by mouth by exchange of saliva, e.g. Epstein-Barr virus, or from contaminated food or water, e.g. Norovirus; by breathing in viruses in the form of aerosols, e.g. Influenza virus; and by insect vectors such as mosquitoes, e.g. dengue. The rate or speed of transmission of viral infections depends on factors that include population density, the number of susceptible individuals, (i.e. those who are not immune),[63] the quality of health care and the weather.[64]

Epidemics and pandemics

The reconstructed 1918 influenza virus

Native American populations were devastated by contagious diseases, particularly smallpox, brought to the Americas by European colonists. It is unclear how many Native Americans were killed by foreign diseases after the arrival of Columbus in the Americas, but the numbers have been estimated to be close to 70% of the indigenous population. The damage done by this disease significantly aided European attempts to displace and conquer the native population.[65][66][67][68][69][70][71]

A pandemic is a world-wide epidemic. The 1918 flu pandemic, commonly referred to as the Spanish flu, was a category 5 influenza pandemic caused by an unusually severe and deadly Influenza A virus. The victims were often healthy young adults, in contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients.
The Spanish flu pandemic lasted from 1918 to 1919. Older estimates say it killed 40–50 million people,[72] while more recent research suggests that it may have killed as many as 100 million people, or 5% of the world's population in 1918.[73]

The Ebola virus

Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century;[74] it is now a pandemic, with an estimated 38.6 million people now living with the disease worldwide.[75] As of January 2006, the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on June 5, 1981, making it one of the most destructive epidemics in recorded history.[76]

Several highly lethal viral pathogens are members of the Filoviridae. Filoviruses are filament-like viruses that cause viral hemorrhagic fever, and include the Ebola and Marburg viruses. The Marburg virus attracted widespread press attention in April 2005 for an outbreak in Angola. Beginning in October 2004 and continuing into 2005, the outbreak was the world's worst epidemic of any kind of viral hemorrhagic fever.[77]

Viruses and cancer

Human leukaemia cells infected by the Epstein Barr virus

Viruses are an established cause of malignancy in humans and other species. The main viruses associated with human cancers are human papillomavirus, hepatitis B and hepatitis C virus, Epstein-Barr virus, and human T-lymphotropic virus. Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver cancer.[78][79] Infection by human T-lymphotropic virus can lead to tropical spastic paraparesis and adult T-cell leukemia.[80] Human papillomaviruses are an established cause of cancers of cervix, skin, anus, and penis.[81] Within the Herpesviridae, Kaposi's sarcoma-associated herpesvirus causes Kaposi's sarcoma and body cavity lymphoma, and Epstein–Barr virus causes Burkitt's lymphoma, Hodgkin’s lymphoma, B lymphoproliferative disorder and nasopharyngeal carcinoma.[82]

Laboratory diagnosis

Cells infected with Herpes simplex virus. The rounding of the cells, their detachment from the cell sheet is the typical cytopathic effect produced by this virus.

In the diagnostic laboratory, virus infections are confirmed by several methods that include:

  • Growth of the virus in a cell culture from a specimen taken from the patient.
  • Detection of virus-specific IgM antibody (see below) in the blood.
  • Detection of virus antigens by ELISA in tissues and fluids.
  • Detection of virus encoded DNA and RNA by PCR.
  • Observation of virus particles by electron microscopy.

Prevention and treatment

Because viruses use the machinery of a host cell to reproduce and reside within them, they are difficult to eliminate without killing the host cell. The most effective medical approaches to viral diseases so far are vaccinations to provide resistance to infection, and antiviral drugs which treat the symptoms of viral infections.

Host immune response

The body's first line of defense against viruses is the innate immune system. This comprises cells and other mechanisms that defend the host from infection in a non-specific manner. This means that the cells of the innate system recognize, and respond to, pathogens in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host.[83]

RNA interference is an important innate defense against viruses.[84] Many viruses have a replication strategy that involves double-stranded RNA dsRNA. When such a virus infects a cell, it releases its RNA molecule or molecules, which immediately bind to a protein complex called Dicer that cuts the RNA into smaller pieces. A biochemical pathway called the RISC complex is activated which degrades the viral mRNA and the cell survives the infection. Rotaviruses avoid this mechanism by not uncoating fully inside the cell and by releasing newly produced mRNA through pores in the particle's inner capsid. The genomic dsRNA remains protected inside the core of the virion.[85][86]

When the adaptive immune system of a vertebrate encounters a virus, it produces specific antibodies which bind to the virus and render it non-infectious. This is called humoral immunity. Two types of antibodies are important. The first called IgM is highly effective at neutralizing viruses but is only produced by the cells of the immune system for a few weeks. The second, called, IgG is produced indefinitely. The presence of IgM in the blood of the host is used to test for acute infection, whereas IgG indicates an infection sometime in the past.[87] Both types of antibodies are measured when tests for immunity are carried out.[88]

A second defense of vertebrates against viruses is called cell-mediated immunity and involves immune cells known as T cells. The body's cells constantly display short fragments of their proteins on the cell's surface, and if a T cell recognizes a suspicious viral fragment there, the host cell is destroyed by T killer cells and the virus-specific T-cells proliferate. Cells such as the macrophage are specialists at this antigen presentation.[89][90]

Not all virus infections produce a protective immune response in this way. HIV evades the immune system by constantly changing the amino acid sequence of the proteins on the surface of the virion. These persistent viruses evade immune control by sequestration, blockade of antigen presentation, cytokine resistance, evasion of natural killer cell activities, escape from apoptosis, and antigenic shift.[91] Other viruses, called "neurotropic viruses", are disseminated by neural spread where the immune system may be unable to reach them.

The production of interferon is an important host defense mechanism.[92]

Vaccines

Vaccination is a cheap and effective way of preventing infections by viruses. Vaccines were used to prevent viral infections long before the discovery of the actual viruses. Their use has resulted in a dramatic decline in morbidity (illness) and mortality (death) associated with viral infections such as polio, measles, mumps and rubella.[93] Smallpox infections have been eradicated.[94] Currently vaccines are available to prevent over thirteen viral infections of humans,[95] and more are used to prevent viral infections of animals.[96] Vaccines can consist of live-attenuated or killed viruses, or viral proteins (antigens).[97] Live vaccines contain weakened forms of the virus that causes the disease. Such viruses are called attenuated. Live vaccines can be dangerous when given to people with a weak immunity, (who are described as immunocompromised), because in these people, the weakened virus can cause the original disease.[98] Biotechnology and genetic engineering techniques are used to produce subunit vaccines. These vaccines use only the capsid proteins of the virus. Hepatitis B vaccine is an example of this type of vaccine.[99] Subunit vaccines are safe for immunocompromised patients because they cannot cause the disease.[100] The Yellow Fever virus vaccine, a live-attenuated strain called 17D, is arguably the safest and most effective vaccine ever generated.

Antiviral drugs

The true DNA base thymidine

File:Zidovudine.svg

Over the past twenty years, the development of antiviral drugs has increased rapidly. This has been driven by the AIDS epidemic. Antiviral drugs are often nucleoside analogues, (fake DNA building blocks), which viruses incorporate into their genomes during replication. The life-cycle of the virus is then halted because the newly synthesized DNA is inactive. This is because these analogues lack the hydroxyl groups which along with phosphorus atoms, link together to form the strong "backbone" of the DNA molecule. This is called DNA chain termination.[101] Examples of nucleoside analogues are aciclovir for Herpes virus infections and lamivudine for HIV and Hepatitis B virus infections. Aciclovir is one of the oldest and most frequently prescribed antiviral drugs.[102]

File:Aciclovir.svg Other antiviral drugs in use target different stages of the viral life cycle. HIV is dependent on a proteolytic enzyme called the HIV-1 protease for it to become fully infectious. There is a class of drugs called protease inhibitors which have been designed to inactivate the enzyme.

Hepatitis C is caused by an RNA virus. In 80% of people infected, the disease is chronic, and without treatment, they are infected and infectious for the remainder of their lives. However, there is now an effective treatment using the nucleoside analogue drug ribavirin combined with interferon.[103] The treatment of chronic carriers of the Hepatitis B virus by using a similar strategy using lamivudine is being developed.[104]

Notable examples

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The clinically most notable[105] virus species belong to the following families:

Comparison table of clinically important virus families and species
Family Baltimore group Important species[106] envelopment[106] Virion shape[106] Replication site[106]
Adenoviridae dsDNA adenovirus non-enveloped icosahedral nucleus
Picornaviridae +ssRNA coxsackievirus, hepatitis a virus, poliovirus non-enveloped icosahedral
Herpesviridae dsDNA epstein-barr virus, herpes simplex virus, type 1 and 2, human cytomegalovirus, human herpesvirus, type 8, varicella zoster virus enveloped nucleus
Hepadnaviridae dsDNA and ssDNA hepatitis B virus enveloped icosahedral nucleus
Flaviviridae +ssRNA hepatitis C virus enveloped icosahedral
Retroviridae +ssRNA human immunodeficiency virus (HIV) enveloped
Orthomyxoviridae -ssRNA influenza virus enveloped spherical nucleus[107]
Paramyxoviridae -ssRNA measles virus, mumps virus, parainfluenza virus, respiratory syncytial virus enveloped spherical
Papovaviridae ssDNA papillomavirus non-enveloped icosahedral
Rhabdoviridae -ssRNA rabies virus enveloped helical, bullet shaped
Reoviridae dsRNA Rotavirus non-enveloped icosahedral cytoplasm
Togaviridae +ssRNA Rubella virus enveloped icosahedral

Applications

Life sciences and medicine

Viruses are important to the study of molecular and cellular biology as they provide simple systems that can be used to manipulate and investigate the functions of cells. The study and use of viruses have provided valuable information about aspects of cell biology. For example, viruses have been useful in the study of genetics and helped our understanding of the basic mechanisms of molecular genetics, such as DNA replication, transcription, RNA processing, translation, protein transport, and immunology.

Gene therapy using an Adenovirus vector

Geneticists often use viruses as vectors to introduce genes into cells that they are studying. This is useful for making the cell produce a foreign substance, or to study the effect of introducing a new gene into the genome. In similar fashion, virotherapy uses viruses as vectors to treat various diseases, as they can specifically target cells and DNA. It shows promising use in the treatment of cancer and in gene therapy. Eastern European scientists have used phage therapy as an alternative to antibiotics for some time, and interest in this approach is increasing, due to the high level of antibiotic resistance now found in some pathogenic bacteria.[108]

Granulosis (GV) and nucleo-polyhedrosis viruses (NPV) may also be used as biological insecticides (e.g. Cydia pomonella granulovirus).

Materials science and nanotechnology

Current trends in nanotechnology promise to make much more versatile use of viruses. From the viewpoint of a materials scientist, viruses can be regarded as organic nanoparticles.[109] Their surface carries specific tools designed to cross the barriers of their host cells. The size and shape of viruses, and the number and nature of the functional groups on their surface, is precisely defined. As such, viruses are commonly used in materials science as scaffolds for covalently linked surface modifications. A particular quality of viruses is that they can be tailored by directed evolution. The powerful techniques developed by life sciences are becoming the basis of engineering approaches towards nanomaterials, opening a wide range of applications far beyond biology and medicine.[110]

Because of their size, shape, and well-defined chemical structures, viruses have been used as templates for organizing materials on the nanoscale. Recent examples include work at the Naval Research Laboratory in Washington, DC, using Cowpea Mosaic Virus (CPMV) particles to amplify signals in microarray based sensors. In this application, the virus particles separate the fluorescent dyes used for signaling in order to prevent the formation of non-fluorescent dimers that act as quenchers.[111] Another example is the use of CPMV as a nanoscale breadboard for molecular electronics.[112] In April 2006, scientists at the Massachusetts Institute of Technology (MIT) created nanoscale metallic wires using a genetically-modified virus.[113] The MIT team was able to use the virus to create a working battery with an energy density up to three times more than current materials. The potential exists for this technology to be used in liquid crystals, solar cells, fuel cells, and other electronics in the future.

Weapons

The ability of viruses to cause devastating epidemics in human societies has led to the concern that viruses could be weaponized for biological warfare. Further concern was raised by the successful recreation of the infamous 1918 influenza virus in a laboratory.[114] The smallpox virus devastated numerous societies throughout history before its eradication. It currently exists in several secure laboratories in the world, and fears that it may be used as a weapon are not totally unfounded. The vaccine for smallpox is not safe, and during the years before the eradication of smallpox disease more people became seriously ill as a result of vaccination than did people from smallpox[115] and smallpox vaccination is no longer universally practiced.[116] Thus, the modern global human population has almost no established resistance to smallpox; if it were to be released, a massive loss of life could be sustained before the virus is brought under control.

Electron micrographs of viruses

See also


References

  1. 1.0 1.1 "virus". The Online Etymology Dictionary. Retrieved 2007-07-16.
  2. 2.0 2.1 "virulent, a." The Oxford English Dictionary - Online. Retrieved 2007-07-16.
  3. "viral, a." The Oxford English Dictionary - Online. Retrieved 2007-07-16.
  4. Paul GF. (1971) A History of Poliomyelitis. Yale University Press: New Haven and London.
  5. Abdul Nasser Kaadan (2007), Al-Razi on Smallpox and Measles, FSTC
  6. George Sarton, Introduction to the History of Science.
    (cf. Dr. A. Zahoor and Dr. Z. Haq (1997), Quotations From Famous Historians of Science, Cyberistan.
  7. 7.0 7.1 Ibrahim B. Syed, Ph.D. (2002). "Islamic Medicine: 1000 years ahead of its times", Journal of the Islamic Medical Association 2, p. 2-9.
  8. David W. Tschanz, MSPH, PhD (August 2003). "Arab Roots of European Medicine", Heart Views 4 (2).
  9. Behbehani AM (1983). "The smallpox story: life and death of an old disease". Microbiol Rev. 47 (4): 455–509. PMID 6319980.
  10. Horzinek MC (1997). "The birth of virology". Antonie van Leeuwenhoek. 71: 15&ndash, 20. doi:10.1023/A:1000197505492.
  11. Chung, King-Thom and Ferris, Deam Hunter (1996). Martinus Willem Beijerinck (1851-1931): pioneer of general microbiology. AMS News 62, 539-543. http://www.asm.org/ASM/files/CCLIBRARYFILES/FILENAME/0000000251/621096p539.pdf PDF]
  12. href="http://encyclopedia.jrank.org/Cambridge/entries/067/Frederick-William-Twort.html">Frederick William Twort
  13. Stanley WM, Loring HS (1936). "THE ISOLATION OF CRYSTALLINE TOBACCO MOSAIC VIRUS PROTEIN FROM DISEASED TOMATO PLANTS". 83 (2143): 85. doi:10.1126/science.83.2143.85. PMID 17756690.
  14. Stanley WM, Lauffer MA (1939). "DISINTEGRATION OF TOBACCO MOSAIC VIRUS IN UREA SOLUTIONS". 89 (2311): 345–347. doi:10.1126/science.89.2311.345. PMID 17788438.
  15. Tsugita A, Gish DT, Young J, Fraenkel-Conrat H, Knight CA, Stanley WM (1960). "THE COMPLETE AMINO ACID SEQUENCE OF THE PROTEIN OF TOBACCO MOSAIC VIRUS". Proc. Natl. Acad. Sci. U.S.A. 46 (11): 1463–9. PMID 16590772.
  16. Pennazio S (2006). "The origin of phage virology". Riv. Biol. 99 (1): 103–29. PMID 16791793.
  17. Goodpasture EW, Woodruff AM, Buddingh GJ (1931). "THE CULTIVATION OF VACCINE AND OTHER VIRUSES IN THE CHORIOALLANTOIC MEMBRANE OF CHICK EMBRYOS". 74 (1919): 371–372. doi:10.1126/science.74.1919.371. PMID 17810781.
  18. Rosen FS (2004). "Isolation of poliovirus--John Enders and the Nobel Prize". N. Engl. J. Med. 351 (15): 1481–3. doi:10.1056/NEJMp048202. PMID 15470207.
  19. Holmes EC, Drummond AJ. The evolutionary genetics of viral emergence.Curr Top Microbiol Immunol. 2007;315:51-66.
  20. Liu Y, Nickle DC, Shriner D, Jensen MA, Learn GH Jr, Mittler JE, Mullins JI. Molecular clock-like evolution of human immunodeficiency virus type 1.Virology. 2004 Nov 10;329(1):101-8.
  21. 21.0 21.1 21.2 21.3 21.4 21.5 21.6 21.7 Prescott, L (1993). Microbiology. Wm. C. Brown Publishers. 0-697-01372-3.
  22. Keese P, Gibbs A. Plant viruses: master explorers of evolutionary space.Curr Opin Genet Dev. 1993 Dec;3(6):873-7.
  23. Koonin EV. The Biological Big Bang model for the major transitions in evolution.Biol Direct. 2007 Aug 20;2:21.
  24. Rybicki EP (1990) The classification of organisms at the edge of life, or problems with virus systematics. S Aft J Sci 86:182-186
  25. LWOFF A (1957). "The concept of virus". J. Gen. Microbiol. 17 (2): 239–53. PMID 13481308.
  26. LWOFF A, HORNE RW, TOURNIER P (1962). "A virus system.". C. R. Hebd. Seances Acad. Sci. (in French). 254: 4225–7. PMID 14467544.
  27. LWOFF A, HORNE R, TOURNIER P (1962). "A system of viruses". Cold Spring Harb. Symp. Quant. Biol. 27: 51–5. PMID 13931895.
  28. Virus Taxonomy 8th Reports of the International Committee on Taxonomy of Viruses C.M. Fauquet, M.A. Mayo, J. Maniloff, U. Desselberger, and L.A. Ball (eds) Academic Press, 1162 pp. (2005) Elsevier Publication Date: 27 May 2005
  29. Baltimore D (1974). "The strategy of RNA viruses". Harvey Lect. 70 Series: 57–74. PMID 4377923.
  30. Temin HM, Baltimore D (1972). "RNA-directed DNA synthesis and RNA tumor viruses". Adv. Virus Res. 17: 129–86. PMID 4348509.
  31. van Regenmortel MH, Mahy BW (2004). "Emerging issues in virus taxonomy". Emerging Infect. Dis. 10 (1): 8–13. PMID 15078590.
  32. Mayo MA (1999). "Developments in plant virus taxonomy since the publication of the 6th ICTV Report. International Committee on Taxonomy of Viruses". Arch. Virol. 144 (8): 1659–66. PMID 10486120.
  33. de Villiers EM, Fauquet C, Broker TR, Bernard HU, zur Hausen H (2004). "Classification of papillomaviruses". Virology. 324 (1): 17–27. doi:10.1016/j.virol.2004.03.033. PMID 15183049.
  34. CASPAR DL, KLUG A (1962). "Physical principles in the construction of regular viruses". Cold Spring Harb. Symp. Quant. Biol. 27: 1–24. PMID 14019094.
  35. CRICK FH, WATSON JD (1956). "Structure of small viruses". Nature. 177 (4506): 473–5. PMID 13309339.
  36. "Virus triangulation numbers via Internet Archive". Retrieved 2006-04-05.
  37. Long GW, Nobel J, Murphy FA, Herrmann KL, and Lourie B (1970) Experience with electron microscopy in the differential diagnosis of smallpox. Applied Microbiology 20(3):497-504.
  38. Kiselev NA, Sherman MB, Tsuprun VL (1990). "Negative staining of proteins". Electron Microsc. Rev. 3 (1): 43–72. PMID 1715774.
  39. 39.0 39.1 39.2 Flinth (2004). Principles of Virology (2nd edn ed.). ASM Press, New York. 1-55581-259-7. Unknown parameter |coauthors= ignored (help)
  40. Pressing J, Reanney DC. Divided genomes and intrinsic noise.J Mol Evol. 1984;20(2):135-46.
  41. Goudsmit, Jaap. Viral Sex. Oxford Univ Press, 1998.ISBN-13: 9780195124965 ISBN-10: 0195124960
  42. Zhou NN, Senne DA, Landgraf JS, Swenson SL, Erickson G, Rossow K, Liu L, Yoon K, Krauss S, Webster RG. Genetic reassortment of avian, swine, and human influenza A viruses in American pigs.J Virol. 1999 Oct;73(10):8851-6.
  43. Worobey M, Holmes EC (1999). "Evolutionary aspects of recombination in RNA viruses". J. Gen. Virol. 80 ( Pt 10): 2535–43. PMID 10573145.
  44. Lukashev AN (2005). "Role of recombination in evolution of enteroviruses". Rev. Med. Virol. 15 (3): 157–67. doi:10.1002/rmv.457. PMID 15578739.
  45. Umene K (1999). "Mechanism and application of genetic recombination in herpesviruses". Rev. Med. Virol. 9 (3): 171–82. PMID 10479778.
  46. Pan XP, Li LJ, Du WB, Li MW, Cao HC, Sheng JF. Differences of YMDD mutational patterns, precore/core promoter mutations, serum HBV DNA levels in lamivudine-resistant hepatitis B genotypes B and C. J Viral Hepat. 2007 Nov;14(11):767-74.
  47. Hampson AW, Mackenzie JS. The influenza viruses.Med J Aust. 2006 Nov 20;185(10 Suppl):S39-43.
  48. Nakajima K. The mechanism of antigenic shift and drift of human influenza virus Nippon Rinsho. 2003 Nov;61(11):1897-903.
  49. Hundley F, McIntyre M, Clark B, Beards G, Wood D, Chrystie I, Desselberger U. Heterogeneity of genome rearrangements in rotaviruses isolated from a chronically infected immunodeficient child.J Virol. 1987 Nov;61(11):3365-72.
  50. Metzner KJ. Detection and significance of minority quasispecies of drug-resistant HIV-1. HIV Ther. 2006 Dec;11(4):74-81.
  51. Barman S, Ali A, Hui EK, Adhikary L, Nayak DP (2001). "Transport of viral proteins to the apical membranes and interaction of matrix protein with glycoproteins in the assembly of influenza viruses". Virus Res. 77 (1): 61–9. PMID 11451488.
  52. Rybicki ibid
  53. Holmes EC.PLoS Biol. 2007 Oct 2;5(10):e278. Viral Evolution in the Genomic Age
  54. Shackelton LA, Holmes EC.Phylogenetic evidence for the rapid evolution of human B19 erythrovirus.J Virol. 2006 Apr;80(7):3666-9.
  55. Vlassov, Alexander V. (Jul 2005). "The RNA World on Ice: A New Scenario for the Emergence of RNA Information". Journal of Molecular Evolution 61: 264-273.
  56. Chen C, Chiu Y, Wei F, Koong F, Liu H, Shaw C, Hwu H, Hsiao K (1999). "High seroprevalence of Borna virus infection in schizophrenic patients, family members and mental health workers in Taiwan". Mol Psychiatry. 4 (1): 33–8. PMID 10089006.
  57. Margolis TP, Elfman FL, Leib D, Pakpour N, Apakupakul K, Imai Y, Voytek C. Spontaneous reactivation of herpes simplex virus type 1 in latently infected murine sensory Ganglia.J Virol. 2007 Oct;81(20):11069-74. Epub 2007 Aug 8.
  58. Bertoletti A, Gehring A (2007). "Immune response and tolerance during chronic hepatitis B virus infection". Hepatol. Res. 37 Suppl 3: S331–8. doi:10.1111/j.1872-034X.2007.00221.x. PMID 17931183.
  59. Nguyen VT, McLaws ML, Dore GJ (2007). "Highly endemic hepatitis B infection in rural Vietnam". doi:10.1111/j.1440-1746.2007.05010.x. PMID 17645465.
  60. Rodrigues C, Deshmukh M, Jacob T, Nukala R, Menon S, Mehta A (2001). "Significance of HBV DNA by PCR over serological markers of HBV in acute and chronic patients". Indian journal of medical microbiology. 19 (3): 141–4. PMID 17664817.
  61. Fowler MG, Lampe MA, Jamieson DJ, Kourtis AP, Rogers MF (2007). "Reducing the risk of mother-to-child human immunodeficiency virus transmission: past successes, current progress and challenges, and future directions". Am. J. Obstet. Gynecol. 197 (3 Suppl): S3–9. doi:10.1016/j.ajog.2007.06.048. PMID 17825648.
  62. Sauerbrei A, Wutzler P (2000). "The congenital varicella syndrome". Journal of perinatology : official journal of the California Perinatal Association. 20 (8 Pt 1): 548–54. PMID 11190597.
  63. Garnett GP. Role of herd immunity in determining the effect of vaccines against sexually transmitted disease.J Infect Dis. 2005 Feb 1;191 Suppl 1:S97-106.
  64. Platonov AE (2006). "The influence of weather conditions on the epidemiology of vector-borne diseases by the example of West Nile fever in Russia". Vestn. Akad. Med. Nauk SSSR (in Russian) (2): 25–9. PMID 16544901.
  65. Ranlet P. The British, the Indians, and smallpox: what actually happened at Fort Pitt in 1763? Pa Hist. 2000;67(3):427-41.
  66. Van Rijn K. "Lo! The poor Indian!" colonial responses to the 1862-63 smallpox epidemic inBritish Columbia and Vancouver Island.Can Bull Med Hist. 2006;23(2):541-60.
  67. Patterson KB, Runge T. Smallpox and the Native American.Am J Med Sci. 2002 Apr;323(4):216-22.
  68. Sessa R, Palagiano C, Scifoni MG, di Pietro M, Del Piano M. The major epidemic infections: a gift from the Old World to the New? Panminerva Med. 1999 Mar;41(1):78-84.
  69. Bianchine PJ, Russo TA. The role of epidemic infectious diseases in the discovery of America. Allergy Proc. 1992 Sep-Oct;13(5):225-32.
  70. Hauptman LM. Smallpox and American Indian; Depopulation in Colonial New York. N Y State J Med. 1979 Nov;79(12):1945-9.
  71. Fortuine R. Smallpox decimates the Tlingit (1787). Alaska Med. 1988 May-Jun;30(3):109.
  72. Patterson, KD (1991). "The geography and mortality of the 1918 influenza pandemic". Bull Hist Med. 65 (1): 4–21. PMID 2021692. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  73. Johnson, Niall P. A. S. and Mueller, Juergen, "Updating the Accounts: Global Mortality of the 1918–1920 'Spanish' Influenza Pandemic," Bulletin of the History of Medicine 76 (2002), pp. 105–115.
  74. Gao, F., Bailes, E., Robertson, D. L., Chen, Y., Rodenburg, C. M., Michael, S. F., Cummins, L. B., Arthur, L. O., Peeters, M., Shaw, G. M., Sharp, P. M. and Hahn, B. H. (1999). "Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes". Nature. 397 (6718): 436&ndash, 441. PMID 9989410 doi:10.1038/17130.
  75. UNAIDS (2006). "Overview of the global AIDS epidemic" (PDF). 2006 Report on the global AIDS epidemic (PDF)|format= requires |url= (help). Retrieved 2006-06-08.
  76. Mawar N, Saha S, Pandit A, Mahajan U. The third phase of HIV pandemic: social consequences of HIV/AIDS stigma & discrimination & future needs.Indian J Med Res. 2005 Dec;122(6):471-84. Review.
  77. Towner JS, Khristova ML, Sealy TK, Vincent MJ, Erickson BR, Bawiec DA, HartmanAL, Comer JA, Zaki SR, Stroher U, Gomes da Silva F, del Castillo F, Rollin PE,Ksiazek TG, Nichol ST. Marburgvirus genomics and association with a large hemorrhagic fever outbreak in Angola.J Virol. 2006 Jul;80(13):6497-516.
  78. Koike K (2007). "Hepatitis C virus contributes to hepatocarcinogenesis by modulating metabolic and intracellular signalling pathways". J. Gastroenterol. Hepatol. 22 Suppl 1: S108–11. doi:10.1111/j.1440-1746.2006.04669.x. PMID 17567457.
  79. Hu J, Ludgate L (2007). "HIV-HBV and HIV-HCV coinfection and liver cancer development". Cancer Treat. Res. 133: 241–52. PMID 17672044.
  80. Bellon M, Nicot C (2007). "Telomerase: a crucial player in HTLV-I-induced human T-cell leukemia". Cancer genomics & proteomics. 4 (1): 21–5. PMID 17726237.
  81. Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S (2007). "Human papillomavirus and cervical cancer". Lancet. 370 (9590): 890–907. doi:10.1016/S0140-6736(07)61416-0. PMID 17826171.
  82. Klein E, Kis LL, Klein G (2007). "Epstein-Barr virus infection in humans: from harmless to life endangering virus-lymphocyte interactions". Oncogene. 26 (9): 1297–305. doi:10.1038/sj.onc.1210240. PMID 17322915.
  83. Alberts, Bruce (2002). Molecular Biology of the Cell; Fourth Edition. New York and London: Garland Science. ISBN 0-8153-3218-1. Unknown parameter |coauthors= ignored (help)
  84. Ding SW, Voinnet O. Antiviral immunity directed by small RNAs. Cell. 2007 Aug 10;130(3):413-26.
  85. Patton JT, Vasquez-Del Carpio R, Spencer E (2004). "Replication and transcription of the rotavirus genome". Curr. Pharm. Des. 10 (30): 3769–77. PMID 15579070.
  86. Jayaram H, Estes MK, Prasad BV (2004). "Emerging themes in rotavirus cell entry, genome organization, transcription and replication". Virus Res. 101 (1): 67–81. doi:10.1016/j.virusres.2003.12.007. PMID 15010218.
  87. Greer S, Alexander GJ. Viral serology and detection. Baillieres Clin Gastroenterol. 1995 Dec;9(4):689-721
  88. Laurence JC. Hepatitis A and B immunizations of individuals infected with humanimmunodeficiency virus.Am J Med. 2005 Oct;118 Suppl 10A:75S-83S.
  89. Cascalho M, Platt JL. Novel functions of B cells.Crit Rev Immunol. 2007;27(2):141-51.
  90. Khatri M, Sharma JM. Modulation of macrophages by infectious bursal disease virus.Cytogenet Genome Res. 2007;117(1-4):388-93
  91. Hilleman MR. Strategies and mechanisms for host and pathogen survival in acute and persistent viral infections. Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14560-6. Epub 2004 Aug 5.
  92. Le Page C, Genin P, Baines MG, Hiscott J. Interferon activation and innate immunity.Rev Immunogenet. 2000;2(3):374-86.
  93. Asaria P, MacMahon E (2006). "Measles in the United Kingdom: can we eradicate it by 2010?". BMJ. 333 (7574): 890–5. doi:10.1136/bmj.38989.445845.7C. PMID 17068034.
  94. Lane JM (2006). "Mass vaccination and surveillance/containment in the eradication of smallpox". Curr. Top. Microbiol. Immunol. 304: 17–29. PMID 16989262.
  95. Arvin AM, Greenberg HB (2006). "New viral vaccines". Virology. 344 (1): 240–9. doi:10.1016/j.virol.2005.09.057. PMID 16364754.
  96. Pastoret PP, Schudel AA, Lombard M (2007). "Conclusions--future trends in veterinary vaccinology". Rev. - Off. Int. Epizoot. 26 (2): 489–94, 495–501, 503–9. PMID 17892169.
  97. Palese P (2006). "Making better influenza virus vaccines?". Emerging Infect. Dis. 12 (1): 61–5. PMID 16494719.
  98. Thomssen R (1975). "Live attenuated versus killed virus vaccines". Monographs in allergy. 9: 155–76. PMID 1090805.
  99. McLean AA (1986). "Development of vaccines against hepatitis A and hepatitis B". Rev. Infect. Dis. 8 (4): 591–8. PMID 3018891.
  100. Casswall TH, Fischler B (2005). "Vaccination of the immunocompromised child". Expert review of vaccines. 4 (5): 725–38. doi:10.1586/14760584.4.5.725. PMID 16221073.
  101. Magden J, Kääriäinen L, Ahola T (2005). "Inhibitors of virus replication: recent developments and prospects". Appl. Microbiol. Biotechnol. 66 (6): 612–21. doi:10.1007/s00253-004-1783-3. PMID 15592828.
  102. Mindel A, Sutherland S (1983). "Genital herpes - the disease and its treatment including intravenous acyclovir". J. Antimicrob. Chemother. 12 Suppl B: 51–9. PMID 6355051.
  103. Witthoft T, Moller B, Wiedmann KH, Mauss S, Link R, Lohmeyer J, Lafrenz M,Gelbmann CM, Huppe D, Niederau C, Alshuth U. Safety, tolerability and efficacy of peginterferon alpha-2a and ribavirin in chronic hepatitis C in clinical practice: The German Open Safety Trial. J Viral Hepat. 2007 Nov;14(11):788-96.
  104. Rudin D, Shah SM, Kiss A, Wetz RV, Sottile VM. Interferon and lamivudine vs. interferon for hepatitis B e antigen-positive hepatitis B treatment: meta-analysis of randomized controlled trials.Liver Int. 2007 Nov;27(9):1185-93.
  105. Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-8215-5. Pages 354-366
  106. 106.0 106.1 106.2 106.3 Unless else specified in boxes, the ref is: Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-8215-5. Pages 354-366
  107. Fisher, Bruce; Harvey, Richard P.; Champe, Pamela C. Lippincott's Illustrated Reviews: Microbiology (Lippincott's Illustrated Reviews Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-8215-5. Page 315
  108. Matsuzaki S, Rashel M, Uchiyama J; et al. (2005). "Bacteriophage therapy: a revitalized therapy against bacterial infectious diseases". J. Infect. Chemother. 11 (5): 211–9. doi:10.1007/s10156-005-0408-9. PMID 16258815.
  109. Proceedings of SPIE -- Volume 6413Smart Materials IV, Nicolas H. Voelcker, Editor, 64130F (Dec. 22, 2006). Hybrid organic-inorganic nanoparticles: controlled incorporation of gold nanoparticles into virus-like particles and application in surface-enhanced Raman spectroscopy Marcus Niebert, James Riches, Mark Howes, Charles Ferguson, Robert G. Parton, Anton P. J. Middelberg, Llew Rintoul, and Peter M. Fredericks.Queensland Univ. of Technology (Australia) (published online Dec. 22, 2006)
  110. Fischlechner M, Donath E (2007). "Viruses as Building Blocks for Materials and Devices". Angewandte Chemie International Edition. doi:10.1002/anie.200603445.
  111. Fluorescent signal amplification of carbocyanine dyes using engineered viral nanoparticles. Carissa M. Soto, Amy Szuchmacher Blum, Nikolai Lebedev, Gary J. Vora, Carolyn E. Meador, Angela P. Won, Anju Chatterji, John E. Johnson, and Banahalli R. Ratna, Journal of the American Chemical Society, 128, 5184 (2006).
  112. An Engineered Virus as a Scaffold for Three-Dimensional Self-Assembly on the Nanoscale. Amy Szuchmacher Blum, Carissa M. Soto, Charmaine D. Wilson, Tina L. Brower, Steven K. Pollack, Terence L. Schull, Anju Chatterji, Tianwei Lin, John E. Johnson, Christian Amsinck, Paul Franzon, Ranganathan Shashidhar and Banahalli Ratna, Small, 7, 702 (2005).
  113. "Researchers build tiny batteries with viruses". MIT News Office. Retrieved 2007-04-05.
  114. "Researchers Reconstruct 1918 Pandemic Influenza Virus; Effort Designed to Advance Preparedness". Centers for Disease Control. Retrieved 2007-04-05.
  115. Aragón TJ, Ulrich S, Fernyak S, Rutherford GW (2003). "Risks of serious complications and death from smallpox vaccination: a systematic review of the United States experience, 1963-1968". BMC public health. 3: 26. doi:10.1186/1471-2458-3-26. PMID 12911836.
  116. Weiss MM, Weiss PD, Mathisen G, Guze P (2004). "Rethinking smallpox". Clin. Infect. Dis. 39 (11): 1668–73. doi:10.1086/425745. PMID 15578369.

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