NEW CFS retrovirus research to be funded by NIH

Discussion in 'Fibromyalgia Main Forum' started by Lichu3, Oct 4, 2007.

  1. Lichu3

    Lichu3 New Member

    This is from the CAA October newletter. What's interesting:
    'superantigens' can stimulate very strong immune responses; 400 CFS subjects would be a good-sized study.

    This may be another subgroup of CFS.


    CFS Researcher Gets Grant from NIH to Study Retrovirus

    Brigitte Huber, PhD, of Tufts University School of Medicine in Boston, has been awarded a grant from the National Institutes for Health (NIH) to study the presence of a specific retrovirus (HERV-K18) as a predictor for CFS that follows a viral infection. The grant—jointly funded by the NIH’s National Institutes of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and the Office of Research on Women’s Health (ORWH)—was awarded based on data from Huber’s pilot study, funded for 2 years by the CFIDS Association of America.

    Research shows that Epstein Barr Virus (EBV) induces the HERV-K18 envelope gene to trigger the expression of a specific superantigen. In the Association-funded pilot study, Huber made genetic comparisons between groups of CFS patients with documented evidence of viral infection and healthy control subjects, looking specifically at the presence of certain HERV-K18 alleles that differ in their superantigen activity. This represents a novel genetic aspect of the EBV/CFS association.

    Results of the pilot study showed statistically significant differences in the HERV-K18 alleles of the CFS study subjects versus the control subjects, indicating genetic evidence for the unique etiology of at least one subgroup of CFS patients. It also suggests the possibility of delineating different subtypes of CFS, depending on the clinical history of the patients.

    With the NIH grant, Huber will work to substantiate these pilot results, using a much larger cohort of 400 CFS patients that has been assembled by coinvestigator, Dr. Renee Taylor, a researcher at the University of Illinois in Chicago. According to Dr. Huber, a positive association between CFS and either HERV-K18 alleles or expression patterns could open new avenues for the development of clinical treatments for CFS.

  2. LindaJones

    LindaJones New Member

    Sounds like they are working on it.
  3. jasminetee

    jasminetee Member

    This is the kind of research we need!
    Thanks for sharing.

  4. ladybugmandy

    ladybugmandy Member

    if the superantigen theory is true, why would valcyte work on us?

    or would it?
  5. ladybugmandy

    ladybugmandy Member

    this is fascinating. some researchers believe EBV induces a protein from the retrovirus HERV-K18 env. that can stimaulte all kinds of immune responses responsible for MS and a host of other diseases!

    i have tried to find out where i can get tested for HERV-K19 but there is no test available by the looks of it.

    my CFS started with EBV but all the tests show its latent. i am now wondering if valcyte is really the best option for me, considering my antibodies are not high.

    this is so have a disease where things are always changing. its like chasing a dragon's tail.

    [This Message was Edited on 10/05/2007]
  6. Lichu3

    Lichu3 New Member

    Here is some info about superantigens. It is from an article about Toxic Shock Syndrome (TSS - linked to tampon use in the 1970's) but the idea of how superantigens may behave is what I want to get across.


    Superantigens are a group of proteins (S aureus toxins in the case of TSS) that are able to activate the immune system by bypassing certain steps in the usual antigen-mediated immune response sequence. Superantigens are not processed within the antigen-presenting cell before being presented to T cells. Instead, they bind directly to molecules of the major histocompatibility complex, class II, which requires recognition of only one element of the T-cell receptor (V beta) to trigger a massive T-cell activation (figure 1: not shown). Between 5% and 30% of the entire T-cell population may be activated.

    Conventional antigens activate only about 0.01% to 0.1% of the T-cell population (11,12). Superantigens lead to a massive release of cytokines, especially tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), and IL-6.
  7. mezombie

    mezombie Member

    I've noticed that the NIH these days is more progressive than the CDC. Years ago there was evidence of retroviral activity among CFS patients, but the CDC was unable to reproduce it, and that was that.

    Now that genetic research has started to take off, we may see more of these kind of studies. And if the NIH is true to its word, we will hopefully see more interdisciplinary research that is funded by a number of different NIH Institutes, as was the case here.

    Thanks for your explanation of superantigens, Lichu3.

    This ties neatly in with one of Dr. Klimas' studies which indicated that our flu-like symptoms may be related to over-production of cytokines.
  8. ladybugmandy

    ladybugmandy Member

    hello. does anyone know how you can be tested for HERV K18? does everyone have it? has anyone asked their doctor about this (especially montoya?) can valcyte inhibit the proteins EBV produces when latent, that supposedly transactivate the HERV K18?

    if anyone gets a chance to do this, please keep us posted.

    thank you
  9. acer2000

    acer2000 New Member

    Using the age old tactic of "piggybacking", first montoya publishes, the NYT times article, the Chia press releases, now this... lets hope they get a critical mass of mindshare and so they can continue to get funding and respect. I love it!
  10. Rafiki

    Rafiki New Member

    Thanks so much for this info!

    This is really interesting. Like many others, I tested neg. for mono in the first few weeks of illness then, months later, had soaring titers that my GP said would have been off the charts earlier so he couldn't understand why they were so high months later. I was of course still symptomatic.

    I wonder if they have totally nailed the cause/effect relationship between EVB and Herv-K18 or not.

    I have such mixed feelings about this because I've gotten excited about many, many findings over the past 28 years. But, I am a little bit excited!


    [This Message was Edited on 10/05/2007]
  11. Forebearance

    Forebearance Member

    I'm glad to hear about this study! Thanks for telling us!

  12. Rafiki

    Rafiki New Member

    I'm not sure what you're saying. Are you saying that you don't think these new findings are pertinent? Are you saying that what happened at incline was, perhaps, a unique phenomenon?

    I'm a bit confused... not unusual for me.


    [This Message was Edited on 10/05/2007]
  13. Rafiki

    Rafiki New Member

    Do you think that the HERV-K18 research is irrelevant to CFS because the alleles are a result of active EBV infection?

    What I'm confused about is your take on this new info.

  14. allamerican7

    allamerican7 New Member

    I am in a fog today so here it goes:

    I have been exposed to a lot of mold my entire life....

    but can different molds contribute to this?

    AND DX with EBV type virus before and directly into over ten years of symptoms.........

    Looking for a little more background for some of the comments above...

  15. Rafiki

    Rafiki New Member

    Hi Erik,

    You must think I'm always confused! But, yeah, I'm confused again.

    You wrote:
    "I see people in other countries who weren't even CLOSE to the origins of CFS writing their own views of "what CFS is" and refer me to articles they've written themselves as evidence - as if that is supposed to make me change my mind about what I personally experienced."

    I was born in a hospital in London, England 1 mo. to the day after the beginning of an outbreak of ME among the nursing students in 1952. There were other, better known, outbreaks of ME in the UK in the 1950s, New Zealand (Tapanui flu) 1982/3 and the earliest recorded (I believe) in Southern California in the 1930s.

    Is what happened in Incline the same illness or something distinct and new?

    This gets at the issue of whether or not what has, unfortunately, come to be called "CFS" is actually what has historically been known as ME.

    Thanks for all your time!

    [This Message was Edited on 10/05/2007]
  16. ladybugmandy

    ladybugmandy Member

    hi all. i just spoke to dr. ablashi and he feels huber's HERV study is flawed (i'm paraphrasing) and didn't seem to lend too much credence to it (he gave be some reasons but i can't remember them). everyone seems to want to push their own theories though, but most doctors seem to be on the HHV6 and mycoplasma band wagon at the moment.

  17. Rafiki

    Rafiki New Member

    I've always assumed since the first news reports that the people in Incline had the same thing I had come down with in '79. I was thrilled to hear that what happened to me was happening to others... sorry to be happy that you guys were suffering!

    And, Osler's Web reinforced what I'd always believed.

    I was just confused when you wrote about Incline as though you guys were patients zero, so to speak.

    Personally, I've always assumed we were all in the same confusing boat suffering the same mal de mer.

    I guess I'm just lucky to host all the suspects including active HHV6. I feel like a popular resort for infective agents! Ah well, I never, ever get a cold or flu. I must be a very exclusive resort.

    Please excuse lame attempt at levity. It's the best I can do.

    [This Message was Edited on 10/05/2007]
  18. RunningAntelope

    RunningAntelope New Member

    I am a CFIDS sufferer for 15 years now who studied microbiology and immunology several years ago as an undergrad, as well as a current patient under Dr. Cheney. I believe that Erik has this right on. HHV-6a is probably the main "cause" of CFIDS, at least if this particular set of CFIDS patients experiences the initial severe depression of the immune system known as Idiopathic CD4+ T-lymphocytopenia in addition to all the fatigue, swollen glands, pain, headaches, secondary infections, etc. HHV6a appears to play a synergistic role in catalyzing other Herpes viruses to exert their ill effects, including CMV and EBV. In so much as it has shown this capability, in some of us, it probably does exacerbate the impact of EBV, making the infection worse and the assumed cause of CFIDS in many people.

    Dr. Cheney does believe that HHV6a or something similar to it (perhaps a novel Herpes virus?) may very well be the proximate cause of this illness. I myself have wondered about the connection between AIDS and CFIDS, because the similarities are striking in many of us. In fact, many researchers believe it is HHV6a and not HIV that is the major player in AIDS. I have heard some people refer to HHV6a as the fire and HIV as the gasoline. If that is true, then perhaps, in many of us, HHV6a is the fire and EBV is the gasoline, although, ultimately not lethal the way HIV is in that scenario.

    Dr. Cheney posits an interesting theory in that, the genetic size of HHV6a varies from what is apparently just that particular virus to one that would be exactly the length of that virus combined with HIV. He thinks it is quite possible that somehow HHV6a and HIV exchanged genetic material, and this novel retrovirus may be behind CFIDS for many of us. Interstingly, he is not a strong proponent of anti-viral medications, at least not the hard-core ones you swallow, although I believe he has been testing Valcyte on some of his patients who meet the minimum criteria for a certain degree of HHV6a infection. He does utilize topical cell-signaling factors that he believes should not only raise energy levels and enhance the body's ability to deal with the by-products of oxygen utilization, but also should have universal anti-viral, anti-microbial properties via their impact on the glutathione peroxidase enzyme, which is the most anti-viral process that exists, as I understand it.

    By the way, I sought Dr. Cheney precisely because of his understanding of the disease process in the heart, as I have been experiencing major heart issues related to this illness, as many of us do, known as diastolic dysfunction. Do not quote me on any of this of course, because it is just theory and my best understanding of the situation. But even though, in theory, HHV6 is transmitted easily in saliva, for example, I've always wondered, in my case, if this somehow wasn't sexually transmitted. Cheney doesn't think so, but I've always wondered how other people feel about this or if we should be doing more to raise awareness. I have read anecdotes of others who have experienced the same thing and feel the same way.

    - Bill
    [This Message was Edited on 10/06/2007]
  19. Mikie

    Mikie Moderator

    Studying one pathogen may well provide some info which may help researchers to understand our illnesses but I do not believe that will help find the "Cause" of CFIDS/ME.

    My CFIDS was triggered by a bacterial mycoplasma infection. That said, though, I can look way back into early childhood and see omens of things to come. Does that mean we are genetically predisposed to CFIDS and that any number of things can trigger it? Or, does exposure to an infection, toxin, or stress cause genetic mutations which can be passed down the line? Many of us recovered from several bouts of these illnesses before finally being brought down by one factor.

    Research into these questions usually just generates more questions due to the complexity of our conditions and the possible triggers.

    The govt. sprayed some unknown substance just 30 miles up the Gulf Coast from me in a little town called, Punta Gorda, in the 1950's. There was a cluster outbreak of CFIDS which has been well documented. Incline Village is probably the most well known cluster outbreak but not the only one. There may have been different triggers in different outbreaks.

    It is my own personal belief that our illnesses are a combination of factors, kind of like "the perfect storm." They seem to run in families, which points to a genetic factor, but even withing families, the triggering event can differ among family members.

    It is good that there is more interest in research but I don't think there will be any simple conclusions.

    Love, Mikie
  20. ladybugmandy

    ladybugmandy Member

    i contracted mono 14 years ago when an ex-boyfriend, whom i later learned had become very promiscious, kissed me. i have had CFS ever since and have always suspected that something else was traveling with the EBV..perhaps HHV6A or something else. the HIV/HHV6A theory is interesting and one that i have never heard before.

    i have no real evidence of active EBV or HHV6 virus but i have an extremely high RNase L.

    thank you for the very informative post.


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