Environmental factors are capable of triggering the expression of human endogenous retroviruses and induce an autoimmune response.
Infection can promote the expression of human endogenous retroviruses by molecular mimicry or by functional mimicry. There are additional mechanisms which may control the expression of human endogenous retroviruses, such as epigenetic status of the genome (hypomethylation, histone deacetylation).
Ultraviolet exposure, chemicals/drugs, injury/stress, hormones, all as a single cause or in a concert, may modulate the involvement of human endogenous retroviruses in pathogenic processes.
In the current review we summarize the current knowledge on infections, molecular mimicry, cross-reactivity and epigenetics contribution for trigger human endogenous retroviruses expression and pathogenesis in lupus patients.
[Note: This abstract was distributed via the Co-Cure ME/CFS & FM Listserv with this comment: “One of the current conversations in medical science is regarding which triggers or combination of triggers can set off a pathogenic process when in combination with viruses. Although this specific study focuses on the autoimmune disease Lupus, and the retrovirus referred to is not XMRV, these principles are being applied in many different processes. For example, Dr. Nancy Klimas is reportedly doing research on Gulf War veterans regarding XMRV. Because it can be proven that these veterans were exposed to a number of adverse environmental factors this has many different implications.”]
Source: Lupus, Nov 2009;18(13):1136-43. PMID: 19880559, by Blank M, Shoenfeld Y, Perl A. Center for Autoimmune Diseases, an Department of Medicine B, Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Israel; Division of Rheumatology, Department of Medicine, State University of New York Upstate Medical University, Syracuse, NY, USA. [E-mail: firstname.lastname@example.org]