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New KDM, Lombardi research--HERV

Daffodil

Senior Member
Messages
5,875
i still dont quite understand the outbreaks and unmistakable instances of transmission of CFS.....one might say that these people in one area or one family all had similar gut issues / immune activity / inflammation due to some environmental cause and then getting an acute infection (or whatever) somehow made them all get CFS because it further activated HERV's??

this part seems a little weird. i know there have some rare outbreaks of MS and other autoimmune diseases, but CFS outbreaks weren't all THAT rare and families with mulitple ill members isnt that rare, either. so how is CFS different from lupus or MS?
 

Gijs

Senior Member
Messages
690
i think this finding is the result of the autonomic overdrive i.e. abnormal stressrespons started by (nor) adrenaline. This finding does not fit in a causal model.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
A possibility is that what autoimmune illness you get depends on environmental, and possibly genetic, factors. Thus re environmental factors, all may get leaky gut, but depending on diet, medications, chemicals, etc., that enter the gut, different substances will pass through the leaky gut wall into the bloodstream and therefore trigger the production of different antibodies, and then autoantibodies to body substances similar to the foreign ones, and as they are different antibodies they attack different body systems.

I haven't explored this through research, but it just seems logical and could explain the differences. Genetic factors could include predispositions to leaky gut or to sensitivity to certain substances (e.g. gluten).
 

serg1942

Senior Member
Messages
543
Location
Spain
*** Hi guido,

"@Sergio: Really? What exactly does it explain? I am totally accepting that the presence of strange DNA leads to disturbances once molecules come free, but that's the consequence of an inflammatory disease, not the cause, and it doesn't necessarily lead to medical complaints either."

***the HERV is part of our own genome, and it may cause inflammation by the process explained in the paper (expressing proteins that will act as superagents, causing disruption in the normal process of antigen pressentation), and I think it may be very plausible that it explains the symptoms as well.

*** Hi Valentinj,

"That does seem like something interesting to look for ... but couldn't healthy people have the proteins without the immune reaction to them?"

*** Yes, they do, it's explained in the paper.

*** Well, I'm going to write to some specialists, b/c I would like to solve my doubts about the exact proposed mechanism. If I have success in doing this, I'll report it here. (and please, if someone can try to answer me, go ahead! )

Saluditos,
Sergio
 

Gijs

Senior Member
Messages
690
In addition, I think that researchers like Lombardi and the WPI after the XMRV debacle not be taken seriously. I hope for those researchers that at least the research is carried out professionally this time. This model (HERV) does not explain the symptoms and findings by other researchers. How and what is infected in de nervous system that explains the chronic overstimulated autonomic part or the abnormal stressrespons by (HERV). It makes no sense. I am not so optimistic. It is one of the many abnormalities.
 

lansbergen

Senior Member
Messages
2,512
This model (HERV) does not explain the symptoms and findings by other researchers. How and what is infected in de nervous system that explains the chronic overstimulated autonomic part or the abnormal stressrespons by (HERV). It makes no sense. I am not so optimistic. It is one of the many abnormalities.

I disagree and will not waste my time and energy on a yes no dispute.
 

Guido den Broeder

Senior Member
Messages
278
Location
Rotterdam, The Netherlands
My guess is that it's even normal, rather than abnormal, and always happens when these cells are activated. But I'd welcome more research. We are still missing a factor that explains why some people get ME and others don't, especially in outbreaks.
 

Daffodil

Senior Member
Messages
5,875
i'm concerned as to why they found this in only 8 out of 12 CFS patients and not all of them.

its really neat that PDC problems can result in massive cytokine production and it is also very interesting that PCD's play a big part in activating NK cells....or something...

this is SO over my head lol
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
I'm getting lots of questions about what I think of the paper published by De Meirlier et al. Plasmacytoid dendritic cells in the duodenum of individuals diagnosed with myalgic encephalomyelitis are uniquely immunoreactive to antibodies to human endogenous retroviral proteins. I am not going to evoke all the reasons why I might have a problem with this paper, whatever it says. I have moved on. Much of it is documented elsewhere on this blog.

Taking the paper at face value, problems with it are the tiny sample size, from patients that I hope had very serious GI complaints, compared to the patient population as a whole, since, presumably, they warranted a duodenal biopsy. I would like to take this opportunity to emphasize that I am completely opposed to taking any risk of harming fragile patients with unnecessary procedures in order to study the disease.

There is no reason to do duodenal biopsies on garden variety ME patients, so the patients in this study should have had significant inflammatory bowel disease, not just IBS. The procedure carries a significant risk. A duodenal punch biopsy can result in death.

There is lots of tissue to study without resorting to that. Fresh tissue is harvested all the time for other reasons, there is lots of material to autopsy and lots of specimens in paraffin, which is what was used in this study. My small intestine in paraffin is stored down the street at the local hospital. And plasmacytoid dendritic cells can be harvested from peripheral blood.

The simplest explanation for the findings in this paper is that there was a range of proteins consistent with a generalized activation of HERVs. Many things can transactivate HERVs including recombination events and exposure to exogenous retroviruses. Perhaps they didn't name the HERV because they were all transactivated? This is what you might expect in someone with inflammatory bowel disease. We have no idea whether these people had a neuroimmune disease or not. The fact that they had a range of symptoms that would qualify for a clasification of CFS is neither here nor there. Endogenous retrovirus-K promoter: a landing strip for inflammatory transcription factors?

There are quite a few papers worth reading in the references, but they missed one: Cell-free HTLV-1 infects dendritic cells leading to transmission and transformation of CD4(+) T cells.

I hope they are right. It would set us on a path to catch us up to MS, where we belong. However, the paper is so vague. Antibodies to proteins expressed by a generic HERV. This negative paper was also just published: Human Endogenous Retrovirus-K18 Superantigen Expression and Human Herpesvirus-6 and Human Herpesvirus-7 Viral Loads in Chronic Fatigue Patients. It is very good news for us that this avenue of research is being pursued.

I expect the De Meirleir paper to get shot down or be ignored completely. The scientific world will probably only read it for laughs, considering the source. They didn't find a "real" virus this time, so nobody needs to spend millions of dollars to prove it wrong.

MSRV was ignored for decades, even though it is associated with a more sympathetic disease than ME/CFS. Progress with it has been glacial, revealing the non-urgent, almost lackadaisacal attitude of the biomedical world towards activated HERVs, even one that was shown to produce viral particles over 20 years ago. In either case, there is increasing agreement that HERV W is associated with MS and can transcribe an Env protein which is neuropathogenic.

February 26, 2013 Dr J Deckoff-Jones: http://www.x-rx.net/blog/2013/02/ms-light.html