Antigenic shift

Antigenic shift is the process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains. The term is often applied specifically to influenza, as that is the best-known example, but the process is also known to occur with other viruses, such as visna virus in sheep.[1] Antigenic shift is a specific case of reassortment or viral shift that confers a phenotypic change.

Not to be confused with Antigenic drift, Antigenic variation, or Genetic drift.
NIAID illustration of potential influenza genetic reassortment

Antigenic shift is contrasted with antigenic drift, which is the natural mutation over time of known strains of influenza (or other things, in a more general sense) which may lead to a loss of immunity, or in vaccine mismatch. Antigenic drift occurs in all types of influenza including influenza A, influenza B and influenza C. Antigenic shift, however, occurs only in influenza A because it infects more than just humans.[2] Affected species include other mammals and birds, giving influenza A the opportunity for a major reorganization of surface antigens. Influenza B and C principally infect humans, minimizing the chance that a reassortment will change its phenotype drastically.[3]

Antigenic shift is important for the emergence of new viral pathogens as it is a pathway that viruses may follow to enter a new niche. It could occur with primate viruses and may be a factor for the appearance of new viruses in the human species such as HIV. Note that HIV itself does not undergo reassortment/antegenic shift due to the structure of its genome, but it does recombine freely and via superinfection, so HIV can produce recombinant HIV strains that differ significantly from their ancestors.

Role in the transmission of influenza viruses from non-human animals to people

Influenza A viruses are found in many different animals, including ducks, chickens, pigs, humans, whales, horses, and seals.[3] Influenza B viruses circulate widely principally among humans, though it has recently been found in seals.[4] Flu strains are named after their types of hemagglutinin and neuraminidase surface proteins (of which there are 18 and 9 respectively), so they will be called, for example, H3N2 for type-3 hemagglutinin and type-2 neuraminidase. Some strains of avian influenza (from which all other strains of influenza A are believed to stem[2]) can infect pigs or other mammalian hosts. When two different strains of influenza infect the same cell simultaneously, their protein capsids and lipid envelopes are removed, exposing their RNA, which is then transcribed to mRNA. The host cell then forms new viruses that combine their antigens; for example, H3N2 and H5N1 can form H5N2 this way. Because the human immune system has difficulty recognizing the new influenza strain, it may be highly dangerous, and result in a new pandemic.[3]

Influenza viruses which have undergone antigenic shift have caused the Asian Flu pandemic of 1957, the Hong Kong Flu pandemic of 1968, and the Swine Flu scare of 1976. Until recently, such combinations were believed to have caused the infamous Spanish flu outbreak of 1918 which killed 40~100 million people worldwide. However, more recent research suggests the 1918 pandemic was caused by the antigenic drift of a fully avian virus to a form that could infect humans efficiently.[5][6] The most recent 2009 H1N1 outbreak was a result of antigenic shift and reassortment between human, avian, and swine viruses.[7] One increasingly worrying situation is the possible antigenic shift between avian influenza and human influenza. This antigenic shift could cause the formation of a highly virulent virus.

In the marine ecosystem

In terms of virology, the marine ecosystem has been largely unstudied, but due to its extraordinary volume, high viral density (100 million viruses per mL in coastal waters, 3 million per mL in the deep sea)[8] and high cell lysing rate (as high as 20% on average), marine viruses' antigenic shift and genetic recombination rates must be quite high.[9] This is most striking when one considers that the coevolution of prokaryotes and viruses in the aquatic environment has been going on since before eukaryotes appeared on earth.

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See also

Notes
  1. Narayan, O; Griffin, DE; Chase, J (1977). "Antigenic shift of visna virus in persistently infected sheep". Science. 197 (4301): 376–378. doi:10.1126/science.195339. PMID 195339.)
  2. Treanor, John (15 January 2004). "Influenza vaccine--outmaneuvering antigenic shift and drift". New England Journal of Medicine. 350 (3): 218–220. doi:10.1056/NEJMp038238. PMID 14724300.
  3. Zambon, Maria C. (November 1999). "Epidemiology and pathogenesis of influenza" (PDF). Journal of Antimicrobial Chemotherapy. 44 (Supp B): 3–9. doi:10.1093/jac/44.suppl_2.3. PMID 10877456. Retrieved 9 January 2008.
  4. Carrington, Damian (11 May 2000). "Seals pose influenza threat". BBC.
  5. Aoki, FY; Sitar, DS (January 1988). "Clinical pharmacokinetics of amantadine hydrochloride". Clinical Pharmacokinetics. 14 (1): 35–51. doi:10.2165/00003088-198814010-00003. PMID 3280212.
  6. Johnson, NP; Mueller, J (Spring 2002). "Updating the accounts: global mortality of the 1918-1920 "Spanish" influenza pandemic". Bulletin of the History of Medicine. 76 (1): 105–115. doi:10.1353/bhm.2002.0022. PMID 11875246.
  7. Smith, G. J. D.; Vijaykrishna, D.; Bahl, J.; Lycett, S. J.; Worobey, M.; Pybus, O. G.; Ma, S. K.; Cheung, C. L.; Raghwani, J.; Bhatt, S.; Peiris, J. S. M.; Guan, Y.; Rambaut, A. (2009). "Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic". Nature. 459 (7250): 1122–1125. doi:10.1038/nature08182. PMID 19516283.
  8. Denny, How the Ocean Works: An Introduction to Oceanography (2008). How the Ocean Works (illustrated ed.). Princeton University Press. ISBN 9780691126470.)
  9. Suttle, CA (2007). "Marine viruses — major players in the global ecosystem". Nature Reviews Microbiology. 5 (10): 801–812. doi:10.1038/nrmicro1750. PMID 17853907.

Further reading

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