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). It usually lasts for 4 to 5 days in the primary condition.
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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.[2]
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.[3] An excellent example to profile this distinction is the rabies virus.[4] 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.[5] 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.[citation needed]
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.[6]
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.[7]
See also
References
- ^ Ryan KJ, Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. p. 881. ISBN 978-0-8385-8529-0.
- ^ Burrell CJ, Howard CR, Murphy FA (2017-01-01), Burrell CJ, Howard CR, Murphy FA (eds.), "Chapter 7 - Pathogenesis of Virus Infections", Fenner and White's Medical Virology (Fifth Edition), London: Academic Press, pp. 77–104, doi:10.1016/b978-0-12-375156-0.00007-2, ISBN 978-0-12-375156-0, PMC 7150039
- ^ Cerino A, Bissolati M, Cividini A, Nicosia A, Esumi M, Hayashi N, Mizuno K, Slobbe R, Oudshoorn P, Silini E, Asti M, Mondelli MU (Jan 1997). "Antibody responses to the hepatitis C virus E2 protein: relationship to viraemia and prevalence in anti-HCV seronegative subjects". J Med Virol. 51 (1): 1–5. doi:10.1002/(sici)1096-9071(199701)51:1<1::aid-jmv1>3.3.co;2-3. PMID 8986942.
- ^ Lodmell DL, Dimcheff DE, Ewalt LC (Mar 2006). "Viral RNA in the bloodstream suggests viremia occurs in clinically ill rabies-infected mice". Virus Res. (Submitted manuscript). 116 (1–2): 114–8. doi:10.1016/j.virusres.2005.09.004. PMID 16242805.
- ^ Gribencha SV, Barinsky IF (Jul 1982). "Viraemia in rabies". Acta Virol. 26 (4): 301. PMID 6127940.
- ^ Mulupuri P, Zimmerman JJ, Hermann J, Johnson CR, Cano JP, Yu W, Dee SA, Murtaugh MP (2007-12-10). "Antigen-Specific B-Cell Responses to Porcine Reproductive and Respiratory Syndrome Virus Infection". Journal of Virology. 82 (1): 358–370. doi:10.1128/JVI.01023-07. ISSN 0022-538X. PMC 2224379. PMID 17942527.
- ^ Lai CJ, Goncalvez AP, Men R, Wernly C, Donau O, Engle RE, Purcell RH (Dec 2007). "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. 81 (23): 12766–74. doi:10.1128/jvi.01420-07. PMC 2169078. PMID 17881450.
External links
This page was last edited on 24 January 2024, at 14:17