Jump to content

Antigenic drift: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
Ccevo2011 (talk | contribs)
182 edits
→‎External links: This has no direct links witth population genetics. Why is this here?
Line 76: Line 76:
* [http://www3.niaid.nih.gov/topics/Flu/Research/basic/AntigenicDriftIllustration.htm An illustration of antigenic drift]
* [http://www3.niaid.nih.gov/topics/Flu/Research/basic/AntigenicDriftIllustration.htm An illustration of antigenic drift]
* [http://www.medterms.com/script/main/art.asp?articlekey=26116 A technical definition]
* [http://www.medterms.com/script/main/art.asp?articlekey=26116 A technical definition]
{{popgen}}
{{Virus topics}}
{{Virus topics}}


Revision as of 18:04, 17 November 2011

Not to be confused with antigenic shift or genetic drift.

The immune system recognizes viruses when antigens on the surfaces of virus particles bind to immune receptors that are specific for these antigens. This is similar to a lock recognizing a key. After an infection, the body produces many more of these virus-specific receptors, which prevent re-infection by this particular strain of the virus and produce acquired immunity. Similarly, a vaccine against a virus works by teaching the immune system to recognize the antigens exhibited by this virus. However, viral genomes are constantly mutating, producing new forms of these antigens. If one of these new forms of an antigen is sufficiently different from the old antigen, it will no longer bind to the receptors and viruses with these new antigens can evade immunity to the original strain of the virus. When such a change occurs, people who have had the illness in the past will lose their immunity to the new strain and vaccines against the original virus will also become less effective[clarification needed]. Two processes drive the antigens to change: antigenic drift[1][2] and antigenic shift, antigenic drift being the more common. The rate of antigenic drift is dependent on two characteristics: the duration of the epidemic, and the strength of host immunity. A longer epidemic allows for selection pressure to continue over an extended period of time and stronger host immune responses increase selection pressure for development of novel antigens.[3]

In influenza viruses

In the influenza virus, the two relevant antigens are the surface proteins, hemagglutinin and neuraminidase.[4] The hemagglutinin is responsible for binding and entry into host epithelial cells while the neuraminidase is involved in the process of new virions budding out of host cells.[5] Sites recognized on the hemagglutinin and neraminidase proteins by host immune systems are under constant selective pressure. Antigenic shift allows for evasion of these host immune systems by small mutations in the hemagglutinin and neraminidase genes that make the protein unrecognizable to pre-existing host immunity. [6] Antigenic drift is this continuous process of genetic and antigenic change among flu strains.[7]

In human populations, immune (vaccinated) individuals exert selective pressure for single point mutations in the hemagglutinin gene that increase receptor binding avidity, while naive individuals exert selective pressure for single point mutations that decrease receptor binding avidity. [8] These dynamic selection pressures facilitate the observed rapid evolution in the hemagglutinin gene. Specifically, 18 specific codons in the HA1 domain of the hemagglutinin gene have been identified as undergoing positive selection to change their encoded amino acid. [9] To meet the challenge of antigenic drift, vaccines that confer broad protection against heterovariant strains are needed against seasonal, epidemic and pandemic influenza.[10]

As in all RNA viruses, mutations in influenza occur frequently because the virus' RNA polymerase has no proofreading mechanism, resulting in an error rate between 1x10^-3 and 8x10^-3 substitutions per site per year during viral genome replication.[11] Mutations in the surface proteins allow the virus to elude some host immunity, and the numbers and locations of these mutations that confer the greatest amount of immune escape has been an important topic of study for over a decade.[12][13][14]

Antigenic drift has been responsible for heavier-than-normal flu seasons in the past, like the outbreak of influenza H3N2 variant A/Fujian/411/2002 in the 2003 - 2004 flu season. All influenza viruses experience some form of antigenic drift, but it is most pronounced in the influenza A virus.

Antigenic drift should not be confused with antigenic shift, which refers to reassortment of the virus' gene segments. As well, it is different from random genetic drift, which is an important mechanism in population genetics.

See also

Notes

  1. ^ D. J. D. Earn, J. Dushoff, S. A. Levin (2002). "Ecology and Evolution of the Flu". Trends in Ecology and Evolution. 17 (7): 334–340. doi:10.1016/S0169-5347(02)02502-8.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ A. W. Hampson (2002). "Influenza virus antigens and antigenic drift". Influenza. Elsevier Science B. V. pp. 49–86. ISBN 0444824618. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)
  3. ^ Boni, T (2006). "Epidemic dynamics and antigenic evolution in a single season of influenza A". Proceedings of the Royal Society of Biological Sciences. 273: 1307–1316. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  4. ^ Bouvier NM, Palese P. The biology of influenza viruses. Vaccine. 2008 Sep 12;26 Suppl 4:D49-53. Review. PMID: 19230160
  5. ^ Nelson, M. I. (2007). "The evolution of pandemic influenza". Nature Reviews Genetics. 8: 196–205. Retrieved 13 November 2011. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  6. ^ Hensley, S. E. (30). "Hemagglutinin receptor binding avidity drives influenza A virus antigenic drift". Science. 326: 734–736. Retrieved 13 November 2011. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  7. ^ Taubenberger, Jeffery K. (17). "Influenza virus evolution, host adaptation and pandemic formation". Cell Host & Microbe. 7: 440–451. Retrieved 13 November 2011. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  8. ^ Hensley, S. E. (30). "Hemagglutinin receptor binding avidity drives influenza A virus antigenic drift". Science. 326: 734–736. Retrieved 13 November 2011. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  9. ^ Bush, R. M. (3). "Predicting the evolution of human influenza A". Science. 286: 1921–1925. Retrieved 13 November 2011. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  10. ^ Carrat F, Flahault A. Influenza vaccine: the challenge of antigenic drift. Vaccine. 2007 Sep 28;25(39-40):6852-62. Epub 2007 Aug 3. Review. PMID: 17719149
  11. ^ Taubenberger, Jeffery K. (17). "Influenza virus evolution, host adaptation and pandemic formation". Cell Host & Microbe. 7: 440–451. Retrieved 13 November 2011. {{cite journal}}: Check date values in: |date= and |year= / |date= mismatch (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  12. ^ R. M. Bush, W. M. Fitch, C. A. Bender, N. J. Cox (1999). "Positive selection on the H3 hemagglutinin gene of human influenza virus". Molecular Biology and Evolution. 16 (11): 1457–1465. PMID 10555276.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ W. M. Fitch, R. M. Bush, C. A. Bender, N. J. Cox (1997). "Long term trends in the evolution of H(3) HA1 human influenza type A". Proceedings of the National Academy of Sciences USA. 94 (15): 7712–7718. doi:10.1073/pnas.94.15.7712.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ D. J. Smith, A. S. Lapedes, J. C. de Jong, T. M. Bestebroer, G. F. Rimmelzwaan, A. D. M. E. Osterhaus, R. A. M. Fouchier (2004). "Mapping the antigenic and genetic evolution of influenza virus". Science. 305 (5682): 371–376. doi:10.1126/science.1097211. PMID 15218094.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Further reading

Boni MF. Vaccination and antigenic drift in influenza. Vaccine. 2008 Jul 18;26 Suppl 3:C8-14. Review. PMID: 18773534

Gog JR. The impact of evolutionary constraints on influenza dynamics. Vaccine. 2008 Jul 18;26 Suppl 3:C15-24. Review. PMID: 18773528

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Antigenic_drift&oldid=461143256"