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Virus evolution

Virus evolution is a section of evolutionary biology and virology that focuses on the evolution of viruses . Many viruses , in particular RNA viruses , have a short reproduction period and an increased mutation frequency (one point mutation or more per genome in one round of virus RNA replication). This increased mutation rate, when combined with natural selection , allows viruses to quickly adapt to environmental changes.

Virus evolution is a critical aspect of the epidemiology of viral diseases such as influenza ( orthomyxoviruses ), HIV infection ( Human Immunodeficiency Virus ) and hepatitis (such as hepatitis C virus ). Rapid mutation of viruses also causes problems with the development of effective vaccines and antiviral drugs , as drug resistance mutations occur within a week or a month after starting treatment. One of the main theoretical models for studying viral evolution is the model of quasivids as viral quasivids .

Content

The origin of viruses

A study at the molecular level revealed a connection between viruses infecting the organisms of each of the three life domains and viral proteins that preceded the separation of life domains and therefore belong to the last universal common ancestor . [1] This shows that some viruses appeared in the early stages of the evolution of life, [2] and that viruses could possibly have arisen repeatedly. [3]

There are three classic hypotheses about the origin of viruses:

  • Viruses could once be small cells that parasitize large cells ( degeneration hypothesis [4] [5] or reduction hypothesis [6] );
  • some viruses could come from pieces of DNA or RNA that “escaped” from the genes of large organisms (the vagrancy hypothesis [7] or the fugitive DNA hypothesis );
  • or viruses could evolve from complexes of protein and nucleic acid molecules simultaneously with the appearance of the first cells on earth or earlier (the primary virus hypothesis ). [6] [8]

None of these hypotheses is fully accepted: the degeneration hypothesis does not explain why even the smallest of the cell parasites are so unlike viruses in any respect. The runaway DNA hypothesis does not explain complex capsids and other structures of viral particles. The primary virus hypothesis was quickly rejected, as it contradicts the very definition of viruses that need host cells . [6] Virologists, however, began to review and reassess all three hypotheses. [9] [10] [11]

One of the problems of studying the origin of viruses and their evolution is their high mutation frequency, especially in the case of RNA retroviruses like HIV / AIDS. A recent study based on a comparison of viral protein folding patterns, however, provides some new evidence. Fold Super Families (FSF's) protein folding superfamilies are proteins that have a similar folding structure of the polypeptide chain regardless of the sequence of their amino acids, and they, as shown, can serve as evidence of the phylogeny of viruses. Thus, viral proteins can be divided into 4 superfamilies; based on three branches of the viruses of bacteria, archaea and eukaryotes, together with the fourth superfamily, which seems to indicate that it separated before being divided into three branches. Thus, “the viral proteome reflects the paths of ancient evolutionary history that can be restored using modern bioinformatics approaches.” Anshan Nasir and Gustavo Caetano-Anollés, “This suggests the existence of ancient cell lines common to cells and viruses even before the appearance of the“ last universal cell ancestor ”which gave rise to modern cells. According to our data, long-term selection to reduce the size of the genome and particle size ultimately led to the reduction of virocells to modern viruses Owls (characterized by a complete loss of cell state), while other co-existing cell lines given the diversity of modern cells. " [12] Moreover, a long genetic distance between the superfamily of RNA and DNA suggests that the hypothesis of an RNA world can have new experimental evidence for long-term intermediate period in the evolution of cell life.

Evolution

Viruses do not form fossils in the traditional sense, because they are much smaller than the smallest colloidal particles that form sedimentary rocks, which lead to the fossilization of plants and animals. However, the genomes of many organisms contain endogenous viral elements (EVEs). These DNA sequences are the remains of ancient viral genes and genomes that "invaded" the host germline cells . For example, the genomes of most vertebrate species contain from hundreds to thousands of sequences derived from ancient retroviruses . These endogenous viral elements are a valuable source of retrospective data on the evolutionary history of viruses and have spawned the science of paleovirusology . [13]

To some extent, the evolutionary history of viruses can be deduced from the analysis of modern viral genomes. Mutation rates for many viruses were measured, and the use of a molecular clock allows the timing of the discrepancy to be determined. [14]

Viruses develop by changing old or acquiring new sequences in their RNA (or DNA), some quite quickly, and the most adapted mutants quickly outnumber their less suitable counterparts. In this sense, their evolution is Darwin . [15] The way in which viruses reproduce in host cells makes them particularly susceptible to genetic changes that help accelerate their evolution. [16] RNA viruses are particularly susceptible to mutations. [17] In host cells, error correction mechanisms exist during DNA replication and are deleted during cell division. [17] These important mechanisms prevent the transmission of lethal mutations to offspring. But these mechanisms do not work for RNA, and when the RNA virus replicates in its host cell, changes in its genes sometimes lead to errors, some of which are fatal. A single virus particle can produce millions of progeny viruses in just one replication cycle, so the appearance of just a few “defective" viruses is not a problem. Most mutations are “silent,” and do not lead to any obvious changes in the viral offspring, but some provide benefits that increase their adaptability to environmental conditions. These may be changes in viral particles masking them from identification by cells of the immune system or changes that make antiviral drugs less effective. Both types of such changes occur frequently with HIV . [18]

Many viruses (such as influenza A virus) can “shuffle” their genes with other viruses when two similar strains infect the same cell. This phenomenon is called antigenic variability , and is often the cause of the emergence of new and more virulent strains. Other viruses change more slowly, as mutations in their genes gradually accumulate over time as the genes drift . [nineteen]

Thanks to these mechanisms, new viruses are constantly appearing and constitute a constant challenge to attempts to control the diseases they cause. [20] [21] It is now known that most types of viruses have common ancestors, and although the hypothesis of the “primacy of viruses” has not yet been fully recognized, there is no doubt that thousands of species of modern viruses evolved from less numerous ancient ones. [22] For example, morbilliviruses are a group of closely related but different viruses that infect a wide 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 hyenas; cattle plague virus, which infects cattle and buffalo; and other viruses of seals, porpoises and dolphins. [23] Although it is not possible to prove which of these rapidly developing viruses is the earliest, since such a closely related group of viruses found in such different hosts suggests the possibility of a common ancestor in the past. [24]

See also

  • DNA viruses

Notes

  1. ↑ Mahy, p. 25
  2. ↑ Mahy, p. 26
  3. ↑ Dimmock, NJ Introduction to Modern Virology. - Blackwell Publishing, 2007. - P. 16. - ISBN 1-4051-3645-6 .
  4. ↑ Leppard, p. sixteen
  5. ↑ Sussman, p. eleven
  6. ↑ 1 2 3 Mahy, p. 24
  7. ↑ Sussman, pp. 11-12
  8. ↑ Villarreal, LP Viruses and the Evolution of Life. ASM Press, 2005. ISBN 978-1555813093 .
  9. ↑ Mahy, pp. 362-78
  10. ↑ Forterre P. Giant viruses: conflicts in revisiting the virus concept (English) // Intervirology : journal. - 2010 .-- June ( vol. 53 , no. 5 ). - P. 362-378 . - DOI : 10.1159 / 000312921 . - PMID 20551688 .
  11. ↑ Forterre P., Krupovic M. The origin of virions and virocells: the Escape hypothesis revisited (English) // Viruses: Essential Agents of Life: journal / G. Witzany. - Springer Science + Business Media Dordrecht, Netherlands, 2012. - P. 43-60 . - DOI : 10.1007 / 978-94-007-4899-6_3 .
  12. ↑ Anshan Nasir and Gustavo Caetano-Anollés, “A phylogenomic data-driven exploration of viral origins and evolution” (Science Advances, Vol 1, No. 8, 04 September 2015)
  13. ↑ Emerman M., Malik HS Paleovirology — modern consequences of ancient viruses (Eng.) // PLoS Biology : journal / Virgin, Skip W. .. - 2010 .-- February ( vol. 8 , no. 2 ). - P. e1000301 . - DOI : 10.1371 / journal.pbio.1000301 . - PMID 20161719 .
  14. ↑ Lam TT, Hon CC, Tang JW Use of phylogenetics in the molecular epidemiology and evolutionary studies of viral infections (English) // Critical Reviews in Clinical Laboratory Sciences : journal. - 2010 .-- February ( vol. 47 , no. 1 ). - P. 5-49 . - DOI : 10.3109 / 10408361003633318 . - PMID 20367503 .
  15. ↑ Leppard, p. 273
  16. ↑ Leppard, p. 272
  17. ↑ 1 2 Domingo E., Escarmís C., Sevilla N., Moya A., Elena SF, Quer J., Novella IS, Holland JJ Basic concepts in RNA virus evolution (Eng.) // The FASEB Journal : journal. - Federation of American Societies for Experimental Biology 1996 .-- June ( vol. 10 , no. 8 ). - P. 859-864 . - PMID 8666162 .
  18. ↑ Boutwell CL, Rolland MM, Herbeck JT, Mullins JI, AllenTM Viral evolution and escape during acute HIV-1 infection // The Journal of Infectious Diseases : journal. - 2010 .-- October ( vol. 202 Suppl 2 , no. Suppl 2 ). - P. S309-14 . - DOI : 10.1086 / 655653 . - PMID 20846038 .
  19. ↑ Chen J., Deng YM Influenza virus antigenic variation, host antibody production and new approach to control epidemics (English) // Virology Journal : journal. - 2009. - Vol. 6 . - P. 30 . - DOI : 10.1186 / 1743-422X-6-30 . - PMID 19284639 .
  20. ↑ Fraile A., García-Arenal F. The coevolution of plants and viruses: resistance and pathogenicity (English) // Advances in Virus Research: journal. - 2010 .-- Vol. Advances in Virus Research . - P. 1-32 . - ISBN 9780123745255 . - DOI : 10.1016 / S0065-3527 (10) 76001-2 . - PMID 20965070 .
  21. ↑ Tang JW, Shetty N., Lam TT, Hon KL Emerging, novel, and known influenza virus infections in humans (Eng.) // Infectious Disease Clinics of North America: journal. - 2010 .-- September ( vol. 24 , no. 3 ). - P. 603-617 . - DOI : 10.1016 / j.idc.2010.04.001 . - PMID 20674794 .
  22. ↑ Mahy, pp. 70-80
  23. ↑ Barrett, p. sixteen
  24. ↑ Barrett, p. 24-25

Literature

  • Rinderpest and peste des petits ruminants: virus plagues of large and small ruminants. - Amsterdam: Elsevier Academic Press, 2006 .-- ISBN 0-12-088385-6 .
  • Introduction to Modern Virology. - Blackwell Publishing Limited, 2007. - ISBN 1-4051-3645-6 .
  • Desk Encyclopedia of General Virology. - Oxford: Academic Press, 2009 .-- ISBN 0-12-375146-2 .
  • Topley & Wilson's microbiology and microbial infections. - London: Arnold, 1998 .-- ISBN 0-340-66316-2 .
  • Witzany, Guenther (ed) ;. Viruses: Essential Agents of Life. - Dortrecht: Springer Science and Business Media, 2012 .-- ISBN 978-94-007-4898-9 .
Source - https://ru.wikipedia.org/w/index.php?title=Virus_evolution&oldid=101044551


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Clever Geek | 2019