Neurovirologist Avindra Nath is leading the new NIH intramural study on ME/CFS. Looking through his publications, I found this interesting conference report from last year. Turns out that Nath and others have found preliminary evidence that human endogenous retroviruses are active and causing harm in MS, ALS, and type 1 diabetes. This whole field is very new and very young. However, it's interesting and at some point when patients are speaking with NIH folks someone should ask Nath if he's going to look for activated HERVs in the ME patients. HERVs are sections of DNA we all carry that encode ancient viruses. Not so long ago, someone discovered these viruses could be reactivated and brought back to life. HERVs are difficult to study, but I was surprised to read in this conference report that a phase 2 clinical trial is underway testing an anti-HERV drug in MS. http://mobilednajournal.biomedcentral.com/articles/10.1186/s13100-015-0051-7 (open source paper...free to download) Here's the summary section at the end of the paper: This first iteration of the ‘HERV & Disease’ workshop provided the opportunity to bring together scientists and clinicians with diverse expertise to share data and ideas about the biology of HERVs and the possible impact of these elements in health and disease. The event came more than two decades after the discovery of the first HERV-W element isolated from an MS patient, a finding that has been the subject of much controversy and debate in the community. How could viral elements assimilated within the genome of humans trigger diseases in certain patients but not others? Many laboratories have invested a considerable effort to clarify this issue, yielding important clues acting at different levels. First, recent advances in genomics have started to provide solutions to the technical challenges posed by the genetic complexity and repetitive nature of HERVs in the human genome. This is best illustrated with HERV-K insertions, a growing number of which have now been shown to be polymorphic and to occur at low frequency in the human population. Furthermore, at the geneenvironment interface, there is growing recognition of cross-talks between diverse infectious agents (including non-retroviral viruses) and HERVs and of their interference with inflammatory and cytopathic signaling pathways. This particular role of environmental microbes provides examples of etiopathogenic mechanisms by which non-physiological HERV activation may occur and may have biological effects. This would confer a “hit and run” role for the many infectious factors often but partially associated with these diseases and a central role for HERVs that, once transcriptionally activated, can Nath et al. Mobile DNA (2015) 6:20 Page 8 of 9 trigger and fuel downstream pathogenic cascades leading to specific lesions or cellular dysfunctions. In parallel, diseases associated with the activation of elements of the HERV-W family have now been extended from MS to other inflammatory neurological or neuropsychiatric diseases, at least one other autoimmune disease (T1D) and, partly or in association with other HERVs, in some cancer states. In the case of HERV-K, evidence is mounting for the involvement of the HERV-K envelope protein in the etiopathogenesis of sporadic SLA, which represents a potential breakthrough for our understanding of this and other neurodegenerative diseases. So, this and many other studies on HERVs open exciting prospects as well as new challenges to elucidate multifactorial etiopathogenic pathways and cellular mechanisms underlying the etiology and progression of many poorly understood pathologies. There is great hope that innovative therapies will emerge from this research. In this respect, the good results from early clinical trials (Phase I in healthy volunteers and Phase IIa in MS patients) for the first specific immunotherapy targeting an associated pathogenic HERV protein (references of publications available from the corresponding author), provide encouraging and new perspectives for the patients.