View source for Viral evolution

{{Short description|Subfield of evolutionary biology and virology concerned with the evolution of viruses}}
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'''Viral evolution''' is a subfield of [[evolutionary biology]] and [[virology]] concerned with the [[evolution]] of [[virus]]es.<ref name="Mahy, p. 24">{{harvnb|Mahy|Van Regenmortel|2009|p=24}}</ref><ref name="Villarreal_2005">{{cite book | vauthors = Villarreal LP |title=Viruses and the Evolution of Life |publisher=ASM Press |year=2005 |isbn=978-1-55581-309-3 |doi=10.1128/9781555817626 |oclc=755638822}}</ref> Viruses have short generation times, and many—in particular [[RNA virus]]es—have relatively high [[mutation rate]]s (on the order of one [[point mutation]] or more per [[genome]] per round of replication). Although most viral mutations confer no benefit and often even prove deleterious to viruses, the rapid rate of viral mutation combined with [[natural selection]] allows viruses to quickly adapt to changes in their host environment. In addition, because viruses typically produce many copies in an infected host, mutated genes can be passed on to many offspring quickly. Although the chance of mutations and evolution can change depending on the type of virus (e.g., [[Double stranded DNA virus|double stranded DNA]], [[Double-stranded RNA viruses|double stranded RNA]], or [[Single-stranded DNA virus|single stranded DNA]]), viruses overall have high chances for mutations.<ref name="pmid38372790">{{cite journal |vauthors=Domingo E, Witzany G |title=Quasispecies productivity |journal=Die Naturwissenschaften |volume=111 |issue=2 |pages=11 |date=February 2024 |pmid=38372790 |doi=10.1007/s00114-024-01897-6}}</ref>

Viral evolution is an important aspect of the [[epidemiology]] of viral diseases such as [[influenza]] ([[influenza virus]]), [[AIDS]] ([[HIV]]), and [[hepatitis]] (e.g. [[Hepatitis C virus|HCV]]). The rapidity of viral mutation also causes problems in the development of successful [[vaccine]]s and [[antiviral drug]]s, as [[Resistance to antiviral drugs|resistant mutation]]s often appear within weeks or months after the beginning of a treatment. One of the main theoretical models applied to viral evolution is the [[quasispecies model]], which defines a [[viral quasispecies]] as a group of closely related viral strains competing within an environment.

==Origins==
=== Three classical hypotheses ===
Studies at the molecular level have revealed relationships between viruses infecting organisms from each of the [[three domain theory|three domains of life]], suggesting viral proteins that pre-date the divergence of life and thus infecting the [[last universal common ancestor]].<ref>{{harvnb|Mahy|Van Regenmortel|2009|p=25}}</ref> This indicates that some viruses emerged early in the evolution of life,<ref>{{harvnb|Mahy|Van Regenmortel|2009|p=26}}</ref> and that they have probably arisen multiple times.<ref>{{harvnb|Leppard|Dimmock|Easton|2007|p=[https://archive.org/details/introductiontomo00dimm_306/page/n258 16]}}</ref> It has been suggested that new groups of viruses have repeatedly emerged at all stages of evolution, often through the displacement of ancestral structural and genome replication genes.<ref name=NRM_Krupovic2019>{{cite journal | vauthors = Krupovic M, Dolja VV, Koonin EV | title = Origin of viruses: primordial replicators recruiting capsids from hosts | journal = Nature Reviews. Microbiology | volume = 17 | issue = 7 | pages = 449–458 | date = July 2019 | pmid = 31142823 | doi = 10.1038/s41579-019-0205-6 | s2cid = 169035711 }}</ref>
 
There are three main classical hypotheses<ref name="Krupovic_2019">{{cite journal |vauthors=Krupovic M, Dolja VV, Koonin EV |title=Origin of viruses: primordial replicators recruiting capsids from hosts |journal=Nature Reviews. Microbiology |volume=17 |issue=7 |pages=449–58 |date=July 2019 |pmid=31142823 |doi=10.1038/s41579-019-0205-6|s2cid=256744818 |url=https://hal-pasteur.archives-ouvertes.fr/pasteur-02557191/file/Krupovic_NRMICRO-19-022_MS_v3_clean.pdf }}</ref> that aim to explain the origins of viruses:

; Regressive hypothesis: Viruses may have once been small cells that [[parasitism|parasitized]] larger cells. Over time, genes not required by their parasitism were lost. The bacteria [[rickettsia]] and [[Chlamydia (genus)|chlamydia]] are living cells that, like viruses, can reproduce only inside host cells. They lend support to this hypothesis, as their dependence on parasitism is likely to have caused the loss of genes that enabled them to survive outside a cell. This is also called the "degeneracy hypothesis",<ref name = "Dimmock_2007" />{{rp|16}}<ref name = "Collier_1998" />{{rp|11}} or "reduction hypothesis".<ref name="Mahy_2009" />{{rp|24}}
; Cellular origin hypothesis: Some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism. The escaped DNA could have come from [[plasmid]]s (pieces of naked DNA that can move between cells) or [[transposons]] (molecules of DNA that replicate and move around to different positions within the genes of the cell).<ref name = "Shors_2017" />{{rp|810}} Once called "jumping genes", transposons are examples of [[mobile genetic elements]] and could be the origin of some viruses. They were discovered in maize by [[Barbara McClintock]] in 1950.<ref>{{cite journal|vauthors= McClintock B|title= The origin and behavior of mutable loci in maize|journal= Proceedings of the National Academy of Sciences of the United States of America|volume=36|issue=6|pages= 344–55|date= June 1950|pmid= 15430309|pmc= 1063197|doi= 10.1073/pnas.36.6.344|bibcode= 1950PNAS...36..344M|doi-access= free}}</ref> This is sometimes called the "vagrancy hypothesis",<ref name = "Dimmock_2007" />{{rp|16}}<ref name = "Collier_1998" />{{rp|11–12}} or the "escape hypothesis".<ref name="Mahy_2009">{{cite book | veditors = Mahy WJ, Regenmortel MH |title=Desk Encyclopedia of General Virology |publisher=Academic Press |location=Oxford |year=2009 |isbn=978-0-12-375146-1}}</ref>{{rp|24}}
; Co-evolution hypothesis: This is also called the "virus-first hypothesis"<ref name="Mahy_2009" />{{rp|24}} and proposes that viruses may have evolved from complex molecules of protein and [[nucleic acid]] at the same time that cells first appeared on Earth and would have been dependent on cellular life for billions of years. [[Viroids]] are molecules of RNA that are not classified as viruses because they lack a protein coat. They have characteristics that are common to several viruses and are often called [[Virus classification#Subviral agents|subviral agents]].<ref name = "Dimmock_2007" />{{rp|55}} Viroids are important pathogens of plants.<ref name = "Shors_2017" />{{rp|791}} They do not code for proteins but interact with the host cell and use the host machinery for their replication.<ref name="Tsagris_2008">{{cite journal | vauthors = Tsagris EM, Martínez de Alba AE, Gozmanova M, Kalantidis K | title = Viroids | journal = Cellular Microbiology | volume = 10 | issue = 11 | pages = 2168–79 | date = November 2008 | pmid = 18764915 | doi = 10.1111/j.1462-5822.2008.01231.x | s2cid = 221581424 | doi-access = free }}</ref> The [[hepatitis delta virus]] of humans has an RNA [[genome]] similar to viroids but has a protein coat derived from hepatitis B virus and cannot produce one of its own. It is, therefore, a defective virus. Although hepatitis delta virus genome may replicate independently once inside a host cell, it requires the help of hepatitis B virus to provide a protein coat so that it can be transmitted to new cells.<ref name = "Shors_2017" />{{rp|460}} In similar manner, the [[sputnik virophage]] is dependent on [[mimivirus]], which infects the protozoan ''[[Acanthamoeba]] castellanii''.<ref name="La_Scola_2008">{{cite journal | vauthors = La Scola B, Desnues C, Pagnier I, Robert C, Barrassi L, Fournous G, Merchat M, Suzan-Monti M, Forterre P, Koonin E, Raoult D | title = The virophage as a unique parasite of the giant mimivirus | journal = Nature | volume = 455 | issue = 7209 | pages = 100–04 | date = September 2008 | pmid = 18690211 | doi = 10.1038/nature07218 | bibcode = 2008Natur.455..100L | s2cid = 4422249 }}</ref> These viruses, which are dependent on the presence of other virus species in the host cell, are called "[[Satellite (biology)|satellites]]" and may represent evolutionary intermediates of viroids and viruses.<ref name = "Collier_1998" />{{rp|777}}<ref name = "Dimmock_2007" />{{rp|55–57}}

=== Later hypotheses ===

* '''Chimeric-origins hypothesis:''' Based on the analyses of the evolution of the replicative and structural modules of viruses, a '''chimeric scenario''' for the origin of viruses was proposed in 2019.<ref name=NRM_Krupovic2019/> According to this hypothesis, the replication modules of viruses originated from the primordial genetic pool, although the long course of their subsequent evolution involved many displacements by replicative genes from their cellular hosts. By contrast, the genes encoding major structural proteins evolved from functionally diverse host proteins throughout the evolution of the virosphere.<ref name=NRM_Krupovic2019/> This scenario is distinct from each of the three traditional scenarios but combines features of the Virus-first and Escape hypotheses.

One of the problems for studying viral origins and evolution is the high rate of viral mutation, particularly the case in RNA retroviruses like HIV/AIDS.  A recent study based on comparisons of viral protein folding structures, however, is offering some new evidence.  Fold Super Families (FSFs) are proteins that show similar folding structures independent of the actual sequence of amino acids, and have been found to show evidence of viral [[phylogeny]]. The [[proteome]] of a virus, the '''viral proteome''', still contains traces of ancient evolutionary history that can be studied today.  The study of protein FSFs suggests the existence of ancient cellular lineages common to both cells and viruses before the appearance of the 'last universal cellular ancestor' that gave rise to modern cells. Evolutionary pressure to reduce genome and particle size may have eventually reduced viro-cells into modern viruses, whereas other coexisting cellular lineages eventually evolved into modern cells.<ref>{{cite journal | vauthors = Nasir A, Caetano-Anollés G | title = A phylogenomic data-driven exploration of viral origins and evolution | journal = Science Advances | volume = 1 | issue = 8 | pages = e1500527 | date = September 2015 | pmid = 26601271 | pmc = 4643759 | doi = 10.1126/sciadv.1500527 | bibcode = 2015SciA....1E0527N }}</ref>  Furthermore, the long genetic distance between RNA and DNA FSFs suggests that the [[RNA world|RNA world hypothesis]] may have new experimental evidence, with a long intermediary period in the evolution of cellular life.

Definitive exclusion of a hypothesis on the origin of viruses is difficult to make on Earth given the ubiquitous interactions between viruses and cells, and the lack of availability of rocks that are old enough to reveal traces of the earliest viruses on the planet. From an [[astrobiological]] perspective, it has therefore been proposed that on celestial bodies such as Mars not only cells but also traces of former virions or viroids should be actively searched for: possible findings of traces of virions in the apparent absence of cells could provide support for the virus-first hypothesis.<ref>{{cite journal| vauthors = Janjic A |date=December 2018|title=The Need for Including Virus Detection Methods in Future Mars Missions |url= https://www.liebertpub.com/doi/10.1089/ast.2018.1851|journal=Astrobiology|language=en|volume=18|issue=12|pages=1611–1614|doi=10.1089/ast.2018.1851|issn=1531-1074|bibcode=2018AsBio..18.1611J|s2cid=105299840|url-access=subscription}}</ref>

==Evolution==
[[File:Journal.pbio.1000301.g001.tif|left|thumb|Time-line of [[viral fossil|paleoviruses]] in the human lineage<ref name="pmid20161719">{{cite journal | vauthors = Emerman M, Malik HS | title = Paleovirology--modern consequences of ancient viruses | journal = PLOS Biology | volume = 8 | issue = 2 | pages = e1000301 | date = February 2010 | pmid = 20161719 | pmc = 2817711 | doi = 10.1371/journal.pbio.1000301 | veditors = Virgin SW | doi-access = free }}</ref>]]
Viruses do not form [[fossil]]s in the traditional sense as they are much smaller than the finest [[colloid]]al fragments forming sedimentary rocks that fossilize plants and animals. However, the genomes of many organisms contain [[endogenous viral element]]s (EVEs). These DNA sequences are the remnants of ancient virus genes and genomes that ancestrally 'invaded' the [[Host (biology)|host]] [[germline]]. For example, the genomes of most [[vertebrate]] species contain hundreds to thousands of sequences derived from ancient [[retrovirus]]es.  These [[endogenous viral element|sequences]] are a valuable source of retrospective evidence about the evolutionary history of viruses, and have given birth to the science of [[paleovirology]].<ref name="pmid20161719"/>

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.<ref name="pmid20367503">{{cite journal | vauthors = Lam TT, Hon CC, Tang JW | title = Use of phylogenetics in the molecular epidemiology and evolutionary studies of viral infections | journal = Critical Reviews in Clinical Laboratory Sciences | volume = 47 | issue = 1 | pages = 5–49 | date = February 2010 | pmid = 20367503 | doi = 10.3109/10408361003633318 | s2cid = 35371362 }}</ref>

Viruses evolve through changes in their RNA (or DNA), some quite rapidly, and the best adapted mutants quickly outnumber their less fit counterparts. In this sense their evolution is [[Darwinism|Darwinian]].<ref>{{harvnb|Leppard|Dimmock|Easton|2007|p=273}}</ref> The way viruses reproduce in their host cells makes them particularly susceptible to the genetic changes that help to drive their evolution.<ref>{{harvnb|Leppard|Dimmock|Easton|2007|p=272}}</ref>  The [[RNA virus]]es are especially prone to mutations.<ref name="pmid8666162">{{cite journal | vauthors = Domingo E, Escarmís C, Sevilla N, Moya A, Elena SF, Quer J, Novella IS, Holland JJ | title = Basic concepts in RNA virus evolution | journal = FASEB Journal | volume = 10 | issue = 8 | pages = 859–864 | date = June 1996 | pmid = 8666162 | doi = 10.1096/fasebj.10.8.8666162 | s2cid = 20865732 | doi-access = free }}</ref> In host cells there are mechanisms for correcting mistakes when DNA replicates and these kick in whenever cells divide.<ref name="pmid8666162"/> 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]].<ref name="pmid20846038">{{cite journal | vauthors = Boutwell CL, Rolland MM, Herbeck JT, Mullins JI, Allen TM | title = Viral evolution and escape during acute HIV-1 infection | journal = The Journal of Infectious Diseases | volume = 202 | issue = Suppl 2 | pages = S309–S314 | date = October 2010 | pmid = 20846038 | pmc = 2945609 | doi = 10.1086/655653 }}</ref>
[[File:Morbillivirus phylogeny.png|200px|thumb|right|Phylogenetic tree showing the relationships of [[morbillivirus]]es of different species<ref>{{harvnb|Barrett|Pastoret|Taylor|2006|p=24}}</ref>]]
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 [[antigenic drift]].<ref name="pmid19284639">{{cite journal | vauthors = Chen J, Deng YM | title = Influenza virus antigenic variation, host antibody production and new approach to control epidemics | journal = Virology Journal | volume = 6 | pages = 30 | date = March 2009 | pmid = 19284639 | pmc = 2666653 | doi = 10.1186/1743-422X-6-30 | doi-access = free }}</ref>

Through these mechanisms new viruses are constantly emerging and present a continuing challenge in attempts to control the diseases they cause.<ref name="pmid20965070">{{cite book |vauthors=Fraile A, García-Arenal F |title=The coevolution of plants and viruses: resistance and pathogenicity |chapter=The Coevolution of Plants and Viruses |volume=76 |pages=1–32 |year=2010 |pmid=20965070 |doi=10.1016/S0065-3527(10)76001-2 |series=Advances in Virus Research |isbn=978-0-12-374525-5|url=http://oa.upm.es/6840/ }}</ref><ref name="pmid20674794">{{cite journal | vauthors = Tang JW, Shetty N, Lam TT, Hon KL | title = Emerging, novel, and known influenza virus infections in humans | journal = Infectious Disease Clinics of North America | volume = 24 | issue = 3 | pages = 603–617 | date = September 2010 | pmid = 20674794 | pmc = 7127320 | doi = 10.1016/j.idc.2010.04.001 }}</ref> 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.<ref>{{harvnb|Mahy|Van Regenmortel|2009|pp=70–80}}</ref> The [[morbillivirus]]es, 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.<ref>{{harvnb|Barrett|Pastoret|Taylor|2006|p=16}}</ref> 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 the possibility that their common ancestor is ancient.<ref>{{harvnb|Barrett|Pastoret|Taylor|2006|pp=24–25}}</ref>

===Bacteriophage===
[[Escherichia virus T4]] (phage T4) is a species of [[bacteriophage]] that infects ''[[Escherichia coli]]'' bacteria. It is a double-stranded [[DNA virus]] in the family ''[[Myoviridae]]''.  Phage T4 is an obligate intracellular parasite that reproduces within the host bacterial cell and its progeny are released when the host is destroyed by [[lysis]]. The complete [[genome]] sequence of phage T4 encodes about 300 [[gene product]]s.<ref>{{cite journal | vauthors = Miller ES, Kutter E, Mosig G, Arisaka F, Kunisawa T, Rüger W | title = Bacteriophage T4 genome | journal = Microbiology and Molecular Biology Reviews | volume = 67 | issue = 1 | pages = 86–156, table of contents | date = March 2003 | pmid = 12626685 | pmc = 150520 | doi = 10.1128/MMBR.67.1.86-156.2003 }}</ref>  These virulent viruses are among the largest, most complex viruses that are known and one of the best studied [[model organism]]s. They have played a key role in the development of [[virology]] and [[molecular biology]].  The numbers of reported [[homology (biology)|genetic homologies]] between phage T4 and [[bacteria]] and between phage T4 and [[eukaryote]]s are similar suggesting that phage T4 shares ancestry with both bacteria and eukaryotes and has about equal similarity to each.<ref name="Bernstein1989">{{cite journal | vauthors = Bernstein H, Bernstein C | title = Bacteriophage T4 genetic homologies with bacteria and eucaryotes | journal = Journal of Bacteriology | volume = 171 | issue = 5 | pages = 2265–2270 | date = May 1989 | pmid = 2651395 | pmc = 209897 | doi = 10.1128/jb.171.5.2265-2270.1989 }}</ref>   Phage T4 may have diverged in evolution from a common ancestor of bacteria and eukaryotes or from an early evolved member of either lineage. Most of the phage genes showing homology with bacteria and eukaryotes encode enzymes acting in the ubiquitous processes of [[DNA replication]], [[DNA repair]], [[genetic recombination|recombination]] and [[nucleotide]] synthesis.<ref name = Bernstein1989/>  These processes likely evolved very early.  The adaptive features of the enzymes catalyzing these early processes may have been maintained in the phage T4, bacterial, and eukaryotic lineages because they were established well-tested solutions to basic functional problems by the time these lineages diverged.

== Transmission ==
Viruses have been able to continue their infectious existence due to evolution. Their rapid mutation rates and natural selection has given viruses the advantage to continue to spread. One way that viruses have been able to spread is with the evolution of virus [[Transmission (medicine)|transmission]]. The virus can find a new host through:<ref>{{cite web|url=https://evolution.berkeley.edu/evolibrary/news/071201_adenovirus|title=Evolution from a virus's view|website=evolution.berkeley.edu|date=December 2007 |access-date=2017-11-27}}</ref>

* [[Droplet transmission]]: the virus is spread to a new host through bodily fluids (an example is the influenza virus)<ref>{{cite web|url=https://www.cdc.gov/flu/keyfacts.htm|title=Key Facts About Influenza (Flu) |work=Seasonal Influenza (Flu)  |date=2017-10-16 |publisher=Center for Disease Control |access-date=2017-12-05}}</ref>
* [[Airborne transmission]]: the virus is passed on through the air (an example is [[viral meningitis]])<ref>{{cite web|url=https://www.cdc.gov/meningitis/viral.html|title=Meningitis, Viral  |date=2017-12-04  |publisher=Center for Disease Control |access-date=2017-12-05}}</ref>
* Vector transmission: the virus is picked up by a carrier and brought to a new host (an example is [[viral encephalitis]])<ref>{{cite web|url=https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0024785/|title=Encephalitis |publisher=National Library of Medicine |work=PubMed Health|access-date=2017-12-05}}</ref>
* Waterborne transmission: the virus leaves a host and enters the water, where a new host consumes the water (an example is the [[poliovirus]])<ref name="CDC_2017">{{cite web|url=https://www.cdc.gov/smallpox/index.html|title=Smallpox |publisher=Center for Disease Control |date=2017-07-13 |access-date=2017-12-05}}</ref>
* Sit-and-wait-transmission: the virus is living outside a host for long periods of time (an example is the [[Smallpox|smallpox virus]])<ref name="CDC_2017" />

[[Virulence]], or the harm that the virus does on its host, depends on various factors. In particular, the method of transmission tends to affect how the level of virulence will change over time. Viruses that transmit through [[Vertically transmitted infection|vertical transmission]] (transmission to the offspring of the host) will evolve to have lower levels of virulence. Viruses that transmit through [[horizontal transmission]] (transmission between members of the same species that don't have a parent-child relationship) will usually evolve to have a higher virulence.<ref>{{cite journal | vauthors = Fries I, Camazine S |title=Implications of horizontal and vertical pathogen transmission for honey bee epidemiology |journal=Apidologie |volume=32 |issue=3 |pages=199–214 |date=2001 |doi=10.1051/apido:2001122 |id=hal-00891679 |url=https://hal.archives-ouvertes.fr/hal-00891679/document}}</ref> {{-}}

== See also ==
{{div col}}
* [[DNA virus]]
* [[Earliest known life forms]]
* [[Evolution of the Sacbrood Virus]]
* [[RNA virus]]
* [[Viral classification]]
* [[Viral decay acceleration]]
* [[Viral phylodynamics]]
* [[Viral quasispecies]]
* [[Endothelial Cell Tropism]]{{Div col end}}

== References ==
<ref name = "Collier_1998">{{cite book | vauthors = Collier L, Balows A, Sussman M | date = 1998 | title = Topley and Wilson's Microbiology and Microbial Infections | edition = 9th | volume = 1 | series = Virology | veditors = Mahy B, Collier LA | isbn = 0-340-66316-2 }}</ref>
<ref name = "Dimmock_2007">{{cite book | vauthors = Dimmock NJ, Easton AJ, Leppard K | date = 2007 | title = Introduction to Modern Virology | edition = 6th | publisher = Blackwell Publishing | isbn = 978-1-4051-3645-7 }}</ref>
<ref name = "Krasner_2014">{{cite book | vauthors = Krasner R | title=The microbial challenge: a public health perspective | publisher=Jones & Bartlett Learning | publication-place=Burlington, Mass | year=2014 | isbn=978-1-4496-7375-8 | oclc=794228026 | page=}}</ref>
<ref name = "Shors_2017">{{cite book | vauthors = Shors T | date = 2017 | title = Understanding Viruses | publisher = Jones and Bartlett Publishers | isbn = 978-1-284-02592-7}}</ref>
{{Reflist|colwidth=30em}}

==Bibliography==
{{refbegin}}
* {{cite book | vauthors = Barrett TC, Pastoret PP, Taylor WJ |title=Rinderpest and peste des petits ruminants: virus plagues of large and small ruminants |publisher=Elsevier |year=2006 |isbn=0-12-088385-6 |url=https://www.sciencedirect.com/science/book/9780120883851 }}
* {{cite book | vauthors = Leppard K, Dimmock N, Easton A |title=Introduction to Modern Virology |publisher=Blackwell |year=2007 |isbn=978-1-4051-3645-7 |oclc=65207057 }}
* {{cite book | veditors = Mahy W, Van Regenmortel MH |title=Desk Encyclopedia of General Virology|publisher=Academic Press |year=2009 |isbn=978-0-12-375146-1 }} 
* {{cite book | vauthors = Sussman M, Topley W, Wilson GK, Collier L, Balows A |title=Topley & Wilson's microbiology and microbial infections |publisher=Arnold |year=1998 |isbn=0-340-66316-2 |ref={{harvid|Sussman|Topley|Wilson|1998}}}}
{{refend}}

== Further reading ==
{{refbegin}}
* {{cite journal |vauthors=Gabrić P |title=Impact of Infectious Disease on Humans and Our Origins |journal=Anthropological Review |volume=85 |issue=1 |pages=101–6 |year=2022 |pmid= |doi=10.18778/1898-6773.85.1.07 |url=https://czasopisma.uni.lodz.pl/ar/article/view/12927 |access-date=2023-05-11 |hdl=11089/43149 |hdl-access=free }}{{refend}}

== External links ==
* {{cite web |title=Where Did Viruses Come From? |date=June 12, 2018 |work=[[PBS Eons]] |url=https://www.youtube.com/watch?v=X31g5TB-MRo&list=PLi6K9w_UbfFR_lBRq0PwTwBxQNUsrXRKf&index=2  |archive-url=https://ghostarchive.org/varchive/youtube/20211212/X31g5TB-MRo| archive-date=2021-12-12 |url-status=live}}{{cbignore}}

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