Endogenous retrovirus

"HERV" redirects here. For other uses, see Herv (disambiguation).
Dendrogram of various classes of endogenous retroviruses

Endogenous retroviruses (ERVs) are endogenous viral elements in the genome that closely resemble and can be derived from retroviruses. They are abundant in the genomes of jawed vertebrates, and they comprise up to 5–8% of the human genome (lower estimates of ~1%).[1][2]

ERVs are a vertically inherited proviral sequence and a subclass of a type of gene called a transposon, which can normally be packaged and moved within the genome to serve a vital role in gene expression and in regulation.[3][4] ERVs however lack most transposon functions, are typically not infectious and are often defective genomic remnants of the retroviral replication cycle.[5][6] They are distinguished as germline provirus retroelements due to their integration and reverse-transcription into the nuclear genome of the host cell.

Researchers have suggested that retroviruses evolved from a type of transposon called a retrotransposon, a Class I element;[7] these genes can mutate and instead of moving to another location in the genome they can become exogenous or pathogenic. This means that not all ERVs may have originated as an insertion by a retrovirus but that some may have been the source for the genetic information in the retroviruses they resemble.[8] When integration of viral DNA occurs in the germ-line, it can give rise to an ERV, which can later become fixed in the gene pool of the host population.[1][9]

  1. ^ a b Cite error: The named reference Belshaw2004 was invoked but never defined (see the help page).
  2. ^ Nelson PN, Hooley P, Roden D, Davari Ejtehadi H, Rylance P, Warren P, et al. (October 2004). "Human endogenous retroviruses: transposable elements with potential?". Clinical and Experimental Immunology. 138 (1): 1–9. doi:10.1111/j.1365-2249.2004.02592.x. PMC 1809191. PMID 15373898.
  3. ^ Khodosevich K, Lebedev Y, Sverdlov E (October 2002). "Endogenous retroviruses and human evolution". Comparative and Functional Genomics. 3 (6): 494–498. doi:10.1002/cfg.216. PMC 2448423. PMID 18629260.
  4. ^ Kim FJ, Battini JL, Manel N, Sitbon M (January 2004). "Emergence of vertebrate retroviruses and envelope capture". Virology. 318 (1): 183–191. doi:10.1016/j.virol.2003.09.026. PMID 14972546.
  5. ^ Stoye JP, Boeke JD (1997). "Retrotransposons, Endogenous Retroviruses, and the Evolution of Retroelements". Retroviruses. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press. p. 343. ISBN 9780879695712. PMID 21433351. NBK19468. Retrieved 2021-02-22.
  6. ^ Gifford RJ, Blomberg J, Coffin JM, Fan H, Heidmann T, Mayer J, et al. (August 2018). "Nomenclature for endogenous retrovirus (ERV) loci". Retrovirology. 15 (1): 59. doi:10.1186/s12977-018-0442-1. PMC 6114882. PMID 30153831.
  7. ^ Cite error: The named reference Rebollo12 was invoked but never defined (see the help page).
  8. ^ Cotton, J. (2001). "Retroviruses from retrotransposons". Genome Biology. 2 (2): 6. doi:10.1186/gb-2001-2-2-reports0006. It appears that the transition from nonviral retrotransposon to retrovirus has occurred independently at least eight times, and the source of the envelope gene responsible for infectious ability can now be traced to a virus in at least four of these instances. This suggests that potentially, any LTR retrotransposon can become a virus through the acquisition of existing viral genes.
  9. ^ Johnson WE, Coffin JM (August 1999). "Constructing primate phylogenies from ancient retrovirus sequences". Proceedings of the National Academy of Sciences of the United States of America. 96 (18): 10254–10260. Bibcode:1999PNAS...9610254J. doi:10.1073/pnas.96.18.10254. PMC 17875. PMID 10468595.