Introduction to viruses: Difference between revisions

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; Regressive theory : Viruses may have once been small cells that [[parasitism|parasitised]] larger cells. Eventually, the genes they no longer needed for a parasitic way of life were lost. The bacteria ''[[Rickettsia]]'' and ''[[Chlamydia (bacterium)|Chlamydia]]'' are living cells that, like viruses, can reproduce only inside host cells. This lends credence to this theory, as their dependence on being parasites may have led to the loss of the genes that once allowed them to live on their own.<ref>{{harvnb|Collier|Balows|Sussman|1998|p=11}}</ref>

; Cellular origin theory : 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 DNA that can move between cellscells—while others may have evolved from bacteria.<ref>{{harvnb|Collier|Balows|Sussman|1998|pp=11–12}}</ref>

; Coevolution theory : Viruses may have evolved from complex molecules of protein and DNA at the same time as cells first appeared on earth, and would have depended on cellular life for many millions of years.<ref name =Wessner>{{cite journal | vauthors = Wessner DR | year = 2010 | title = The Origins of Viruses | journal = Nature Education | volume = 3 | issue = 9| page = 37 }}</ref>

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== Effects on the host cell ==

Viruses have an extensive range of structural and biochemical effects on the host cell.{{sfn | Oxford |Kellam|Collier| 2016 | p=34–36}} These are called ''[[cytopathic effect]]s''.{{sfn | Oxford |Kellam|Collier| 2016 | p=34}} Most virus infections eventually result in the death of the host cell. The causes of death include cell lysis (bursting), alterations to the cell's surface membrane and [[apoptosis]] (cell "suicide").<ref name="pmid28846635">{{cite journal |vauthors=Okamoto T, Suzuki T, Kusakabe S, Tokunaga M, Hirano J, Miyata Y, Matsuura Y |title=Regulation of Apoptosis during Flavivirus Infection |journal=Viruses |volume=9 |issue=9 |pages= 243|year= 2017 |pmid=28846635 |pmc=5618009 |doi=10.3390/v9090243|doi-access=free }}</ref> Often cell death is caused by cessation of its normal activity due to proteins produced by the virus, not all of which are components of the virus particle.<ref name="pmid18637511">{{cite journal <!--Deny Citation Bot-->|vauthors=Alwine JC |title=Modulation of host cell stress responses by human cytomegalovirus |journal=Current Topics in Microbiology and Immunology |volume=325|pages=263–79 |date=2008 |pmid=18637511 |doi=10.1007/978-3-540-77349-8_15}}</ref>

Some viruses cause no apparent changes to the infected cell. Cells in which the virus is [[virus latency|latent]] (inactive) show few signs of infection and often function normally.<ref name="pmid18164651">{{cite journal | vauthors = Sinclair J | title = Human cytomegalovirus: Latency and reactivation in the myeloid lineage | journal = J. Clin. Virol. | volume = 41 | issue = 3 | pages = 180–185 | date = March 2008 | pmid = 18164651 | doi = 10.1016/j.jcv.2007.11.014 }}</ref> This causes persistent infections and the virus is often dormant for many months or years. This is often the case with [[herpes simplex|herpes viruses]].<ref name="pmid6326635">{{cite journal | vauthors = Jordan MC, Jordan GW, Stevens JG, Miller G | title = Latent herpesviruses of humans | journal = Ann. Intern. Med. | volume = 100 | issue = 6 | pages = 866–880 | date = June 1984 | pmid = 6326635 | doi = 10.7326/0003-4819-100-6-866 }}</ref><ref name="pmid12076064">{{cite journal | vauthors = Sissons JG, Bain M, Wills MR | s2cid = 24879226 | title = Latency and reactivation of human cytomegalovirus | journal = J. Infect. | volume = 44 | issue = 2 | pages = 73–77 | date = February 2002 | pmid = 12076064 | doi = 10.1053/jinf.2001.0948}}</ref>