First international workshop on HERVs & disease 2015

[natasa778]

...
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.

... at the gene-environment 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 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. ...

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.

http://www.mobilednajournal.com/content/6/1/20

 

[Research 1st]

HERV's are detected in ME gut tissue with deep sequencing. These aren't unique to ME and found in other autoimmune diseases. A positive aspect to this, is what is 'found' isn't new to science (being present in other autoimmune diseases) and thus won't be disputed to the level as if an exogenous retrovirus was detected.

Yet we have an odd situation in terms of presenting the evidence of putative pathogens then associated to autoimmunity and this potential breakthrough helping the patients gain legitimacy.

Currently, we're messing around with finding autoimmunity (effect of disease) in ME patients but not presenting the pathogen (enabler of disease). Effect is OK, cause is what you want. A proposed cause, would of course be highly controversial, and if proven, a finding of monumental proportions ,perhaps as we're talking congenital Lyme (ultra controversial) in slow onset adolescent ME or autoimmune Lyme (controversial as this would 'prove' Chronic Lyme isn't Lyme but an autoimmune disease from contact with Borrelia or it's co-infections/viruses.

As patient's we all waiting in limbo. The pathogen that apparently causes this needs years worth of further research, so they won't publish on the HERV findings until they're totally certain of the pathogen's presence, presumably because a secondary effect of these HERV's is the possible association with dementia. That will again, take years worth of more research and from multiple groups in various countries.

The people on our side know the proverbial will hit the fan by the 'enemy' rolling out the Fukuda and F48.0 psych patients when any 'cause' of ME is proposed and they know a 'no association with pathogen X' will be the result, from this when you go anywhere near 'CFS' or 'ME', not using a biomarker. in a highly heterogenous group of symptom based patients - aka CFS/ME.

Autoimmunity, gives you a biomarker.

So the people on our side must prove if you have the autoimmune disease, then you must have the pathogen, before they can publish. That then proves causation if 100% of the patients with the autoimmunity always are infected, and never, without.

That's the benefit of us having to sit here for years more and years and years waiting and waiting and waiting because the government science agencies are funding CBT GET and mind-body, not pathogen studies.

It looks logical that HERV's is where it is in ME, but as you've noticed, no studies are funded, because they won't go anywhere near this idea because of who caused it. Themselves.

 

[Asa]

That's the benefit of us having to sit here for years more and years and years waiting and waiting and waiting because the government science agencies are funding CBT GET and mind-body, not pathogen studies.

It looks logical that HERV's is where it is in ME, but as you've noticed, no studies are funded, because they won't go anywhere near this idea because of who caused it. Themselves.

Because I was curious: According to the website below, and for the UK at least, over 75% of CBT therapists and over 75% of physiotherapists are women. And these job sectors are forcasted to grow, grow, grow...

http://web.archive.org/web/20151020...es/Pages/Cognitive-behavioural-therapist.aspx

http://web.archive.org/web/20151020...anning/jobprofiles/Pages/physiotherapist.aspx