Viewing a single comment thread. View all comments

supapoopascoopa t1_jcjvu3o wrote

Endogenous retroviruses are defective, only vertically transmitted like other genes, and none yet found are competent to produce virions. But they are all in some sense heritable infections and also “infect” new cells every time a cell divides.

Some can produce proteins and even entire viral like particles using host machinery. These proteins are associated with autoimmune diseases and certain cancers. One could argue these are “active” infections in terms of causing symptoms.

The takehome message as usual is that nature in general and viruses in particular don’t give a hoot about arbitrary definitions.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187282

142

Reisevi3ber t1_jclq4q5 wrote

Which ones can cause autoimmune diseases and cancers?

14

Uncynical_Diogenes t1_jcm6cq8 wrote

“Which ones” is probably not a super stellar question because they probably have quite boring technical names, and the list of ones we actually have found and named is likely much smaller than the list of potential causative agents.

References 4-7 of the linked text:

> 4. Boller K, Konig H, Sauter M, et al. Evidence that HERV-K is the endogenous retrovirus sequence that codes for the human teratocarcinoma-derived retrovirus HTDV. Virology 1993;196:349–53. [PubMed] [Google Scholar]

>5. Lower R, Boller K, Hasenmaier B, et al. Identification of human endogenous retroviruses with complex mRNA expression and particle formation. Proc Natl Acad Sci U S A 1993;90:4480–4. [PMC free article] [PubMed] [Google Scholar]

>6. Nelson PN. Retroviruses in rheumatic diseases. Ann Rheum Dis 1995;55:441–2. [PMC free article] [PubMed] [Google Scholar]

>7. Nelson PN, Lever AML, Smith S, et al. Molecular investigations implicate human endogenous retroviruses as mediators of anti-retroviral antibodies in autoimmune rheumatic disease. Immunol Invest 1999;28:277–89. [PubMed] [Google Scholar]

Some rheumatic conditions and at least one cancer have been at least linked to expression of human ERV’s, if not necessarily the causative agents of such.

21