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Viral evolution

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Viral evolution is a subfield of evolutionary biology and virology that is specifically concerned with the evolution of viruses. Many viruses, in particular RNA viruses, have short generation times and relatively high mutation rates (on the order of one point mutation or more per genome per round of replication for RNA viruses). This elevated mutation rate, when combined with natural selection, allows viruses to quickly adapt to changes in their host environment.

Viral evolution is an important aspect of the epidemiology of viral diseases such as influenza (influenza virus), AIDS (HIV), and hepatitis (e.g. HCV). It also causes problems in the development of successful vaccines and antiviral drugs, as resistant mutations often appear within weeks or months after the beginning of the treatment. One of the main theoretical models to study viral evolution is the quasispecies model, as the viral quasispecies.

Origins

Viruses are ancient. Studies at the molecular level have revealed relationships between viruses infecting organisms from each of the three domains of life and viral proteins that pre-date the divergence of life and thus the last universal common ancestor.[1] This indicates that some viruses emerged early in the evolution of life,[2] and that viruses have probably arisen multiple times.[3]

There are three classical hypotheses on the origins of viruses: Viruses may have once been small cells that parasitised larger cells (the degeneracy hypothesis[4][5] or reduction hypothesis[6]); some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism (the vagrancy hypothesis[7] or escape hypothesis); or viruses could have evolved from complex molecules of protein and nucleic acid at the same time as cells first appeared on earth (the virus-first hypothesis).[6]

None of these hypotheses was fully accepted: the regressive hypothesis did not explain why even the smallest of cellular parasites do not resemble viruses in any way. The escape hypothesis did not explain the complex capsids and other structures on virus particles. The virus-first hypothesis was quickly dismissed because it contravened the definition of viruses, in that they require host cells.[6] Virologists are, however, beginning to reconsider and re-evaluate all three hypotheses.[8][9][10]

Evolution

Time-line of paleoviruses in the human lineage[11]

Viruses do not form fossils in the traditional sense, because they are much smaller than the grains of sedimentary rocks that fossilize plants and animals. However, the genomes of many organism contain endogenous viral elements (EVEs). These DNA sequences are the remnants of ancient virus genes and genomes that ancestrally 'invaded' the host germline. For example, the genomes of most vertebrate species contain hundreds to thousands of sequences derived from ancient retroviruses. These sequences are a valuable source of retrospective evidence about the evolutionary history of viruses, and have given birth to the science of paleovirology.[11]

The evolutionary history of viruses can to some extent be inferred from analysis of contemporary viral genomes. The mutation rates for many viruses have been measured, and application of a molecular clock allows dates of divergence to be inferred.[12]

Viruses evolve through changes in their DNA (or RNA), some quite rapidly, and the best adapted mutants quickly outnumber their less fit counterparts. In this sense their evolution is Darwinian, just like that of their host organisms.[13] The way viruses reproduce in their host cells makes them particularly susceptible to the genetic changes that help to drive their evolution.[14] The RNA viruses are especially prone to mutations.[15] In host cells there are mechanisms for correcting mistakes when DNA replicates and these kick in whenever cells divide.[15] These important mechanisms prevent potentially lethal mutations from being passed on to offspring. But these mechanisms do not work for RNA and when an RNA virus replicates in its host cell, changes in their genes are occasionally introduced in error, some of which are lethal. One virus particle can produce millions of progeny viruses in just one cycle of replication, therefore the production of a few "dud" viruses is not a problem. Most mutations are "silent" and do not result in any obvious changes to the progeny viruses, but others confer advantages that increase the fitness of the viruses in the environment. These could be changes to the virus particles that disguise them so they are not identified by the cells of the immune system or changes that make antiviral drugs less effective. Both of these changes occur frequently with HIV.[16]

Phylogenetic tree showing the relationships of morbilliviruses of different species[17]

Many viruses (for example, influenza A virus) can "shuffle" their genes with other viruses when two similar strains infect the same cell. This phenomenon is called genetic shift, and is often the cause of new and more virulent strains appearing. Other viruses change more slowly as mutations in their genes gradually accumulate over time, a process known as genetic drift.[18]

Through these mechanisms new viruses are constantly emerging and present a continuing challenge to attempts to control the diseases they cause.[19][20] Most species of viruses are now known to have common ancestors, and although the "virus first" hypothesis has yet to gain full acceptance, there is little doubt that the thousands of species of modern viruses have evolved from less numerous ancient ones.[21] The morbilliviruses, for example, are a group of closely related, but distinct viruses that infect a broad range of animals. The group includes measles virus, which infects humans and primates; canine distemper virus, which infects many animals including dogs, cats, bears, weasels and hyaenas; rinderpest, which infected cattle and buffalo; and other viruses of seals, porpoises and dolphins.[22] Although it is not possible to prove which of these rapidly evolving viruses is the earliest, for such a closely related group of viruses to be found in such diverse hosts suggests a possible ancient common ancestor.[23]

See also

References

  1. ^ Mahy, p. 25
  2. ^ Mahy, p. 26
  3. ^ Dimmock, N.J. (2007). Introduction to Modern Virology. Blackwell Publishing. p. 16. ISBN 1-4051-3645-6.
  4. ^ Leppard, p. 16
  5. ^ Sussman, p. 11
  6. ^ a b c Mahy, p. 24
  7. ^ Sussman, pp. 11–12
  8. ^ Mahy, pp. 362–78
  9. ^ Forterre P (June 2010). "Giant viruses: conflicts in revisiting the virus concept". Intervirology. 53 (5): 362–78. doi:10.1159/000312921. PMID 20551688.
  10. ^ Forterre P, Krupovic M (2012). G. Witzany (ed.). "The origin of virions and virocells: the Escape hypothesis revisited". Viruses: Essential Agents of Life. Springer Science+Business Media Dordrecht, Netherlands: 43–60.
  11. ^ a b Emerman M, Malik HS (February 2010). Virgin, Skip W. (ed.). "Paleovirology—modern consequences of ancient viruses". PLoS Biology. 8 (2): e1000301. doi:10.1371/journal.pbio.1000301. PMC 2817711. PMID 20161719.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ Lam TT, Hon CC, Tang JW (February 2010). "Use of phylogenetics in the molecular epidemiology and evolutionary studies of viral infections". Critical Reviews in Clinical Laboratory Sciences. 47 (1): 5–49. doi:10.3109/10408361003633318. PMID 20367503.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Leppard, p. 273
  14. ^ Leppard, p. 272
  15. ^ a b Domingo E, Escarmís C, Sevilla N, Moya A, Elena SF, Quer J, Novella IS, Holland JJ (June 1996). "Basic concepts in RNA virus evolution". The FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology. 10 (8): 859–64. PMID 8666162.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Boutwell CL, Rolland MM, Herbeck JT, Mullins JI, Allen TM (October 2010). "Viral evolution and escape during acute HIV-1 infection". The Journal of Infectious Diseases. 202 Suppl 2 (Suppl 2): S309–14. doi:10.1086/655653. PMC 2945609. PMID 20846038.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Barrett, p. 24
  18. ^ Chen J, Deng YM (2009). "Influenza virus antigenic variation, host antibody production and new approach to control epidemics". Virology Journal. 6: 30. doi:10.1186/1743-422X-6-30. PMC 2666653. PMID 19284639.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  19. ^ Fraile A, García-Arenal F (2010). "The coevolution of plants and viruses: resistance and pathogenicity". Advances in Virus Research. Advances in Virus Research. 76: 1–32. doi:10.1016/S0065-3527(10)76001-2. ISBN 9780123745255. PMID 20965070.
  20. ^ Tang JW, Shetty N, Lam TT, Hon KL (September 2010). "Emerging, novel, and known influenza virus infections in humans". Infectious Disease Clinics of North America. 24 (3): 603–17. doi:10.1016/j.idc.2010.04.001. PMID 20674794.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Mahy, pp. 70–80
  22. ^ Barrett, p. 16
  23. ^ Barrett, p. 24–25

Bibliography

  • Barrett, Thomas C; Pastoret, Paul-Pierre; Taylor, William J.; (2006). Rinderpest and peste des petits ruminants: virus plagues of large and small ruminants. Amsterdam: Elsevier Academic Press. ISBN 0-12-088385-6.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  • Leppard, Keith; Nigel Dimmock; Easton, Andrew (2007). Introduction to Modern Virology. Blackwell Publishing Limited. ISBN 1-4051-3645-6.{{cite book}}: CS1 maint: multiple names: authors list (link)
  • Desk Encyclopedia of General Virology. Oxford: Academic Press. 2009. ISBN 0-12-375146-2. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)
  • Sussman, Max; Topley, W. W. C.; Wilson, Graham K.; Collier, L. H.; Balows, Albert (1998). Topley & Wilson's microbiology and microbial infections. London: Arnold. ISBN 0-340-66316-2.{{cite book}}: CS1 maint: multiple names: authors list (link)
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