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


Viremia is a medical condition where viruses enter the bloodstream and hence have access to the rest of the body. It is similar to bacteremia, a condition where bacteria enter the bloodstream.[1] The name comes from combining the word virus with the Greek word for blood (haima).

Primary versus Secondary

Primary viremia refers to the initial spread of virus in the blood from the first site of infection.

Secondary viremia occurs when primary viremia has resulted in infection of additional tissues via bloodstream, in which the virus has replicated and once more entered the circulation.

Usually secondary viremia results in higher viral shedding and viral loads within the bloodstream due to the possibility that the virus is able to reach its natural host cell from the bloodstream and replicate more efficiently than the initial site.[2] An excellent example to profile this distinction is the rabies virus.[3] Usually the virus will replicate briefly within the first site of infection, within the muscle tissues. Viral replication then leads to viremia and the virus spreads to its secondary site of infection, the Central nervous system (CNS). Upon infection of the CNS, secondary viremia results and symptoms usually begin.[4] Vaccination at this point is useless, as the spread to the brain is unstoppable. Vaccination must be done before secondary viremia takes place for the individual to avoid brain damage or death.

Active versus Passive

Active viremia is caused by the replication of viruses which results in viruses being introduced into the bloodstream. Examples include the measles, in which primary viremia occurs in the epithelial lining of the respiratory tract before replicating and budding out of the cell basal layer (viral shedding), resulting in viruses budding into capillaries and blood vessels.[5]

Passive viremia is the introduction of viruses in the bloodstream without the need of active viral replication. Examples include direct inoculation from mosquitoes, through physical breaches or via blood transfusions.[6]

See also


  1. Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. p. 881. ISBN 0-8385-8529-9.
  2. Cerino A, Bissolati M, Cividini A, Nicosia A, Esumi M, Hayashi N, Mizuno K, Slobbe R, Oudshoorn P, Silini E, Asti M, Mondelli MU. "Antibody responses to the hepatitis C virus E2 protein: relationship to viraemia and prevalence in anti-HCV seronegative subjects." J Med Virol. 1997 Jan;51(1):1-5.
  3. Lodmell DL, Dimcheff DE, Ewalt LC. "Viral RNA in the bloodstream suggests viremia occurs in clinically ill rabies-infected mice." Virus Res. 2006 Mar;116(1-2):114-8. Epub 2005 Oct 19.
  4. Gribencha SV, Barinsky IF. "Viraemia in rabies." Acta Virol. 1982 Jul;26(4):301.
  5. Mulupuri P, Zimmerman JJ, Hermann J, Johnson CR, Cano JP, Yu W, Dee SA, Murtaugh MP. "Antigen-Specific B-cell Responses to Porcine Reproductive and Respiratory Syndrome Virus Infection." J Virol. 2007 Oct 17
  6. Lai CJ, Goncalvez AP, Men R, Wernly C, Donau O, Engle RE, Purcell RH. "Epitope determinants of a chimpanzee dengue virus type 4 (DENV-4)-neutralizing antibody and protection against DENV-4 challenge in mice and rhesus monkeys by passively transferred humanized antibody." J Virol. 2007 Dec;81(23):12766-74. Epub 2007 Sep 19.

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