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Human endogenous retroviruses & neuro disorders - Avindra Nath publication

Discussion in 'Other Health News and Research' started by viggster, Feb 27, 2016.

  1. viggster

    viggster Senior Member

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    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.
     
  2. LisaGoddard

    LisaGoddard Senior Member

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    This is really interesting. My brain is zogged at the moment so will have to come back to read it later.
    Thanks for posting!
     
    viggster likes this.
  3. daisybell

    daisybell Senior Member

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    New Zealand
    This would be a very neat solution to the question about why so many of us report an infectious trigger...
     
  4. A.B.

    A.B. Senior Member

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    Research 1st, leela and catly like this.
  5. viggster

    viggster Senior Member

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    Thanks for sharing that. Interesting, though such a small study. But good to know others have HERVs on their radar.
     
  6. searcher

    searcher

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    I think it's also worth looking into Brigitte Huber's work. I am not sure if her lab at Tufts is still looking at the link between HERVs and CFS. Here is one grant she had looking at EBV, HERVs, and CFS: http://grantome.com/grant/NIH/R01-AR053821-05
     
    pibee, Roy S, Simon and 2 others like this.
  7. Roy S

    Roy S former DC ME/CFS lobbyist

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    Illinois, USA
    Good finds.

    For what it's worth, there was a temporary but amazing effect from a drug combination including an antiretroviral reported by a ME patient on another forum (the whole forum is now gone). She reported it to her unnamed San Francisco Bay area physician who then said other patients were reporting the same thing. Their mental abilities were not just restored; they were better than ever. Her family was telling her it was like something out of the Twilight Zone. Unfortunately it gradually faded away in less than a year.

    I've thought for decades that research on this disease could yield benefits way beyond just us.


    p.s. I want my brain back.
     
    pibee, Michelle, beaker and 11 others like this.
  8. Michelle

    Michelle Decennial ME/CFS patient

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    Portland, OR
    I think I say that several times a day. Often w/tears in my eyes (like right now). If I could have one thing back from all this disease has taken from me, that would be it.

    @viggster Thanks so much for posting this (as well as your contributions to our community!). Seriously fascinating. And I second @searcher 's recommendation about Huber. She been looking at this for awhile now.
     
    Roy S likes this.
  9. Research 1st

    Research 1st Severe ME, POTS & MCAS.

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    Vaccine contaminants are activating the fossil retroviruses, and these are causing neuroimmune and neuropsychiatric diseases in genetically susceptible individuals by activating HERV's in many diseases, ME just one of them.

    Lab created mouse SFFV got into the human population, SFFV is a neurotoxic mouse virus used in cancer research (in mice) to study human disease. BLV in breast cancer (human) presumably came from infected milk from cows carrying these novel infections. SFFV was discussed in the 2009 SCIENCE paper, but not allowed to be prominently featured, but placed in the afterthought section, with the focus on 'XMRV' which didn't exist, not Silverman's variant anyway. SFFV, was then conveniently never discussed again, even though 6% (using flawed study) found it in Americans in 2011. That's the equivalent of many millions of people immune reacting to a LAB created infection walking around in society having sex with people, donating blood, and sneezing on people - a huge alarm bell, but wrapped up nicely in a 'negative paper' that swiftly changed focus to no inflammation and Dr Hornig the psychiatrist (Dr Lipkin's long term colleague) turning up, just in time. (ME is of course associated to chronic high levels of inflammation, even after 30 years, never mind 3 years). However, these inflammatory ME sufferers have retroviruses. The 'fatigue' patients, without the neuro damage associated to ME (Neuropathy, POTS) don't have them, as Cindy Bateman's samples showed.

    The people to blame are the people who never funded you, the state health agencies, not just the Americans who created the absurd notion of a 'CFS' explaining post infections severe disability, and eventual development of non HIV-AIDS. The British also knew decades ago after a drug trial caused the participants to develop irreversible CFS, this is in the MRC files they hid from the public until 2074. They knew patients were dying from 'ME'. Prominent people, established educated people respected in society, hence the 'story' is censored in the MRC files on 'ME/CFS', not just the names of the deceased.

    HERV's are driving the autoimmunity and the HERV's are releasing prions.
    This is why the authorities turn a blind eye to the powerful psychiatrists who create false enemies (delusional trait) in the media (propaganda) whilst trying to garner sympathy in the press for aiding the infection of tens of millions of now disabled people (psychopathy). Without the hatred for the patients, people ask questions what is happening, why are people slowly (very slowly) getting cancer, diabetes, heart failure, neuropathy, who originally had little old innocent 'CFS' in the teenage years, but are now falling apart like an immune compromised host, constantly infected by upper respiratory infections and the women getting PCOS, Fibroids and the men getting Prostate inflammation...because that's what happens in the other 'imagined' disease Chronic Lyme, or should I say, retroviral Lyme.

    Dr Montoya's patient samples were 85% positive for retroviruses but you aren't supposed to ask WHY no one is doing anything from the government other than to clean the blood supply with filter paper that traps retroviruses, we are told in the headlines don't exist. Dr Lipkin won't say, still denies a retroviral link to CFS. No answers will come from him, when people with ME are excluded from his research! (Read the exclusion criteria of the 2011 paper), anyone medically ill, was excluded. They concentrated on unexplained Chronic Fatigue. Not PWME crippled by low grade, chronic, cyclical brain inflammation (ME) amd thus found no difference with the infected lab workers (controls). Hence, no correlation with exogenous retrovirus and CFS. Easy to play that out with enough 'spin'.

    CFS will become a neuropsychiatric disorder, alongside Major Depression and Schizophrenia. The NIH love this, as the do the British MRC who all know the cause, hence they conversations on patients deaths with ME are redacted, at the same time as pushing a cognitive behavioural approach. You can work this 'CFS' tragedy out, without being there by reading what was censored, who censored it, and when. Then you see who is writing the propaganda at the same time in history and being awarded for it. They knew, long ago, that vaccines trigger ME, but instead of coming clean, they buried it, because by researching it, people would have realised reverse transcriptase was found in MS in the 1990's (as well as CFS) and the dots would have been joined twenty years ago to retroviruses in MS as well as CFS. HERV's are also found in ALS (fatal disease) and Sjogren's Syndrome, Cancers etc.

    Dr Montoya's samples are 85% positive for retrovirus, in inflammatory CFS (ME), people with Fukuda CFS fatigue, don't have this, Dr Bateman's samples (Pro SEID doctor) were negative. NIH is seething that Mikovits told everyone the Lipkin paper was rigged, (which it was) by Fauci denying a 3rd round of testing, spling the samples, and not following same methods of detection as was agreed in the study design. She was gagged for 4 years and couldn't tell anyone, so now, time has passed, and the press articles are all over. Exactly what was planned, has occurred.

    Apparently, in the background, elite informed patients with money are taking Antiretrovirals and have been for years, behind our backs (that's what money allows you to do, make choices others cannot). There's even a new drug that's been tested in MS to treat HERV's, which thankfully was safe. HERV's need organising, and it won't be one cause, so it's massively complex for each disease studied.

    HERV's are only 'controversial' because of revealing what is activating them - man.

    The public doesn't know who caused this HERV activation, but they wouldn't care anyway. Too busy paying tax and looking at the news feeds on Bieber and the Kardashians. Due to a human disinterest in what doesn't affect them, a subset of 'CFS' will become autoimmune by 2018, however it will be longer until the 'cause' will be proven for ME. No one will care.

    Mainstream CFS will become a neuropsychiatric disorder, treated with CBT, this allows the perfect get out of jail cause, for the institutions who failed to investigate the original patients with ME, trapped inside CFS/ME. Clever isn't it? But if you know the answers to the questions before the exam, then winning isn't exactly hard.
     
    Last edited: Feb 28, 2016

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