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|journal=J Virol. |month=Oct |pages=12507–14 |volume=79 |issue=19 |pmid=16160178
|journal=J Virol. |month=Oct |pages=12507–14 |volume=79 |issue=19 |pmid=16160178
|doi=10.1128/JVI.79.19.12507-12514.2005
|doi=10.1128/JVI.79.19.12507-12514.2005
|pmc=1211540}}</ref></blockquote>. However, the absence of known infectious members of the HERV-K(HML2) family, and the lack of elements with a full coding potential within the published human genome sequence, suggests to some that the family is less likely to be active at present.
|pmc=1211540}}</ref></blockquote>. Recently it has been suggested that two members of HERV-K(HML2), HERV-K106 and HERV-K116, were active in the last 800,000 years and that HERV-K106 may have infected modern humans 150,000 years ago <ref>{{cite journal
|author=Aashish R. Jha
|coauthors=Douglas F Nixon; Michael G. Rosenberg; Jeffrey N. Martin; Steven G. Deeks; Richard R. Hudson; Keith E. Garrison; Satish K. Pillai
|year=2011 |url=http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0020234
|title=Human Endogenous Retrovirus K106 (HERV-K106) Was Infectious after the Emergence of Anatomically Modern Humans
|journal=PLoS ONE |month=May |pages=e20234|volume=6 |issue=5 |pmid=
|doi=doi:10.1371/journal.pone.0020234}}</ref></blockquote>. However, the absence of known infectious members of the HERV-K(HML2) family, and the lack of elements with a full coding potential within the published human genome sequence, suggests to some that the family is less likely to be active at present.


In 2004 it was reported that antibodies to HERVs were found at greater frequency in the sera of people with [[schizophrenia]]. Additionally, the [[cerebrospinal fluid]] of people with recent onset schizophrenia contained levels of a retroviral marker, [[reverse transcriptase]], four times higher than control subjects.<ref>{{cite journal
In 2004 it was reported that antibodies to HERVs were found at greater frequency in the sera of people with [[schizophrenia]]. Additionally, the [[cerebrospinal fluid]] of people with recent onset schizophrenia contained levels of a retroviral marker, [[reverse transcriptase]], four times higher than control subjects.<ref>{{cite journal

Revision as of 21:40, 26 May 2011

Dendrogram of various classes of endogenous retroviruses

Endogenous retroviruses (ERVs) are sequences in the genome thought to be derived from ancient viral infections of germ cells in humans, mammals and other vertebrates; as such their proviruses are passed on to the next generation and now remain in the genome.

Hypothesis of origin

Endogenous retroviruses may be a variant of a retrovirus which became permanently integrated with its host and is inherited from generation to generation as part of the genome of the host.

Retroviruses are single-stranded RNA viruses that reverse-transcribe their RNA into DNA for integration into the host's genome. Most retroviruses (such as HIV-1) infect somatic cells, but in very rare cases, it is thought that exogenous retroviruses have infected germline cells (cells that make eggs and sperm) allowing integrated retroviral genetic sequences to be passed on to subsequent progeny, thereby becoming 'endogenous'. Endogenous retroviruses have persisted in the genome of their hosts for thousands of years. However, they are generally only infectious for a short time after integration as they acquire many inactivating mutations during host DNA replication. They can also be partially excised from the genome by a process known as recombinational deletion. They are thought to play a key role in evolution.[1] Some human ERVs have been implicated in ALS[2], certain autoimmune diseases, and cancers.[3][4]

Endosymbiotic ERVs in mammals

During pregnancy in viviparous mammals (all mammals except Monotremes), ERVs are activated and produced in high quantities during the implantation of the embryo. They are hypothesised to possess immunosuppressive properties, suggesting a role in gestational immune tolerance, protecting the embryo from its mother's immune system. Production of the envelope protein of a class of ERVs of sheep, the endogenous Jaagsiekte sheep retroviruses (enJSRVs), has been demonstrated to be necessary for maintaining pregnancy[5].

Also, viral fusion proteins apparently cause the formation of the placental syncytium[6] in order to limit the exchange of migratory cells between the developing embryo and the body of the mother (something an epithelium will not do sufficiently, as certain blood cells are specialized to be able to insert themselves between adjacent epithelial cells). An immunoevasive action was the initial normal behavior of the viral protein, in order to avail for the virus to spread to other cells by simply merging them with the infected one (HIV does this too). It is believed that the ancestors of modern viviparous mammals evolved after an infection by this virus, enabling the fetus to better resist the immune system of the mother.[7]

The human genome project found several thousand ERVs classified into 24 families.[8]

Human endogenous retroviruses

Human endogenous retroviruses (HERVs) are suspected of involvement in some autoimmune diseases, in particular with multiple sclerosis. In this disease, there appears to be a specially associated member of the family of human endogenous retrovirus W known as "MS-associated retrovirus" (MSRV).[9] [10]

There are many thousands of endogenous retroviruses within human DNA, with HERVs comprising nearly 8% of the human genome and composed with 98,000 elements and fragments.[11]) According to one study published in 2005, no HERVs capable of replication had been identified; all appeared to be defective, containing major deletions or nonsense mutations. This is because most are just long-lasting traces of the original virus, having first integrated many millions of years ago. However, there is one family of viruses that have been active since the divergence of humans and chimpanzees. This family, termed HERV-K (HML2), makes up less than 1% of HERV elements but is one of the most studied. There are indications it has even been active in the past few hundred thousand years, e.g. some human individuals carry more copies of the virus family than others [12]. Recently it has been suggested that two members of HERV-K(HML2), HERV-K106 and HERV-K116, were active in the last 800,000 years and that HERV-K106 may have infected modern humans 150,000 years ago [13]. However, the absence of known infectious members of the HERV-K(HML2) family, and the lack of elements with a full coding potential within the published human genome sequence, suggests to some that the family is less likely to be active at present.

In 2004 it was reported that antibodies to HERVs were found at greater frequency in the sera of people with schizophrenia. Additionally, the cerebrospinal fluid of people with recent onset schizophrenia contained levels of a retroviral marker, reverse transcriptase, four times higher than control subjects.[14] Researchers continue to look at a possible link between HERVs and schizophrenia, with the additional possibility of a triggering infection inducing schizophrenia.[15]

In 2006, researchers led by Thierry Heidmann at the Institut Gustave Roussy in Villejuif, France were able to recreate a HERV, which they dubbed Phoenix.[16][17]

In 2007, a collaborative group led by Doug Nixon and Keith Garrison at the University of California San Francisco, and by Mario Ostrowski and Brad Jones at the University of Toronto, published a study providing evidence for T cell immune responses against HERVs in human immunodeficiency virus (HIV) infected individuals.[18] The group hypothesized that HIV induces HERV expression in HIV infected cells, and that a vaccine targeting HERV antigens could therefore specifically eliminate HIV infected cells. The potential advantage of this novel approach is that, by using HERV antigens as surrogate markers of HIV infected cells, it could circumvent the difficulty inherent in directly targeting notoriously diverse and rapidly mutating HIV antigens.

See also

References

  1. ^ Ryan FP (2004). "Human endogenous retroviruses in health and disease: a symbiotic perspective". Journal of the Royal Society of Medicine. 97 (12): 560–5. doi:10.1258/jrsm.97.12.560. PMC 1079666. PMID 15574851. {{cite journal}}: Unknown parameter |month= ignored (help)
  2. ^ "Reactivated Virus May Contribute to ALS".
  3. ^ "Demystified . . . Human endogenous retroviruses".
  4. ^ Singh SK (2007). "Endogenous retroviruses: suspects in the disease world". Future Microbiology. 2 (3): 269–75. doi:10.2217/17460913.2.3.269. PMID 17661701. {{cite journal}}: Unknown parameter |month= ignored (help)
  5. ^ Dunlap KA, Palmarini M, Varela M; et al. (2006). "Endogenous retroviruses regulate periimplantation placental growth and differentiation". Proceedings of the National Academy of Sciences. 103 (39): 14390–5. doi:10.1073/pnas.0603836103. PMID 16980413. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ Mi S, Lee X, Li X; et al. (2000). "Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis". Nature. 403 (6771): 785–9. doi:10.1038/35001608. PMID 10693809. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Luis P. Villarreal (2004). "Can Viruses Make Us Human?" (PDF). Proceedings of the American Philosophical Society. 148 (3): 314. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ Luis P. Villarreal (2001). "Persisting Viruses Could Play Role in Driving Host Evolution". ASM News (American Society for Microbiology). {{cite journal}}: Unknown parameter |month= ignored (help)
  9. ^ Mameli G, Astone V, Arru G, Marconi S, Lovato L, Serra C, Sotgiu S, Bonetti B, Dolei A (2007). "Brains and peripheral blood mononuclear cells of multiple sclerosis (MS) patients hyperexpress MS-associated retrovirus/HERV-W endogenous retrovirus, but not human herpesvirus 6". J Gen Virol. 88 (Pt 1): 264–74. doi:10.1099/vir.0.81890-0. PMID 17170460. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ Serra C, Mameli G, Arru G, Sotgiu S, Rosati G, Dolei A (2003). "In vitro modulation of the multiple sclerosis (MS)-associated retrovirus by cytokines: implications for MS pathogenesis". J Neurovirol. 9 (6): 637–43. doi:10.1080/714044485. PMID 14602576. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Robert Belshaw (2004). "Long-term reinfection of the human genome by endogenous retroviruses". Proc Natl Acad Sci USA. 101 (14): 4894–99. doi:10.1073/pnas.0307800101. PMC 387345. PMID 15044706. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  12. ^ Robert Belshaw (2005). "Genomewide Screening Reveals High Levels of Insertional Polymorphism in the Human Endogenous Retrovirus Family HERV-K(HML2): Implications for Present-Day Activity". J Virol. 79 (19): 12507–14. doi:10.1128/JVI.79.19.12507-12514.2005. PMC 1211540. PMID 16160178. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  13. ^ Aashish R. Jha (2011). "Human Endogenous Retrovirus K106 (HERV-K106) Was Infectious after the Emergence of Anatomically Modern Humans". PLoS ONE. 6 (5): e20234. doi:doi:10.1371/journal.pone.0020234. {{cite journal}}: Check |doi= value (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  14. ^ Yolken R. (2004). "Viruses and schizophrenia: a focus on herpes simplex virus". Herpes. 11 (Suppl 2): 83A–88A. PMID 15319094. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. ^ Douglas Fox (June 2010). "The Insanity Virus". Discover. Retrieved February 17, 2011.
  16. ^ Martin Enserink (2006). "Viral Fossil Brought Back to Life". ScienceNOW Daily News. {{cite journal}}: Unknown parameter |month= ignored (help)(news article)
  17. ^ Dewannieux M, Harper F, Richaud A; et al. (2006). "Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements". Genome Res. 16 (12): 1548–56. doi:10.1101/gr.5565706. PMC 1665638. PMID 17077319. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)(original paper)
  18. ^ Garrison KE, Jones RB, Meiklejohn DA; et al. (2007). "T cell responses to human endogenous retroviruses in HIV-1 infection". PLoS Pathog. 3 (11): e165. doi:10.1371/journal.ppat.0030165. PMC 2065876. PMID 17997601. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)

External links

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