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Simmaron Scientist Awarded NIH Grant Probing Cause of Immune Holes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

August 31, 2014

NIH Grant to Study Genetics of Immune Response in ME/CFS

Simmaron Research Foundation’s Scientific Director, Isabel Barao PhD, has been awarded the IDeA Clinical and Translational Research Pilot Grant (CTR-IN) from the National Institutes of Health (NIH) to examine ways ME/CFS patients’ genetic heritage may contribute to immune dysfunction and their inability to fight off viruses. Dr. Peterson will select the patients, collect their blood and provide their clinical information. The laboratory work will be performed at University of Nevada School of Medicine (UNSOM), Department of Microbiology and Immunology, where Dr. Barao is academically affiliated.

DNA

This study will probe genetic holes in natural killer cells

The $75,000 grant is small, but it is an important sign of Simmaron’s ability to advance new investigators involved in immunological research on ME/CFS at the NIH. The CTR-IN grant is supported by the National Institute of General Medical Sciences. The 1-year grant supports 20% of Dr. Barao’s pay and supplies for laboratory work.

Dr. Barao has also submitted an R21 grant proposal to the NIH in collaboration with the National Cancer Institute (NCI), Dr. Peterson and UNSOM.

ME/CFS is believed to be a multi-factorial disorder caused by a combination of one’s genetic makeup, an environmental trigger such as a pathogen, and other factors. It’s believed that 20-40% of the reason people came down with ME/CFS lies in their genes.

Take away that genetic component and maybe that infection that never went away passes on through like every other cold did. Maybe that bout of fatigue that stayed and got worse resolves with rest this time. It may take one factor to tip the system into the situation we call ME/CFS. That factor could lie in our genes.

First Line of Immune Defense Down

This grant will help determine if altered FcRs (e.g. CD16) on natural killer (NK) cells have made it more difficult for ME/CFS patients t0 fight off viruses.  NK cells are the cells our immune system uses to hold the invader at bay while cytotoxic T-cells and B-cells gear up to wipe out the invader.

We know that poorly functioning NK cells could be allowing pathogens to get entrenched more deeply into ME/CFS patients’ systems, perhaps even into immunologically privileged parts of our nervous system that the big guns of our immune system have trouble getting to.

Second Line of Immune Defense Down As Well?

pathogens

Could ME/CFS genetics be giving pathogens the upper hand in ME/CFS?

It turns out, though, that natural killer cells not only play a vital role in the first lines of our immune defense – they also play an important role in fighting off chronic infections. This study suggests NK cell problems in ME/CFS may also be allowing chronic viral infections to persist.

During an infection, B-cells start pumping out IgG antibodies that attach to and stop pathogens from infecting our cells. Once IgG antibodies have attached to a pathogen, NK cells are able to recognize, attack and kill cells infected with pathogens through FcRs, using a process called ‘antibody-dependent cell-mediated cytotoxicity’ (ADCC).

Studies have shown that individuals with genetic alterations (polymorphisms) of the genes associated with that ADCC response have an increased risk of cancer and autoimmune disorders. Genetic impairment of the ADCC response could also make it more difficult to clear herpes viral infections, which are of such interest in ME/CFS.

A Talk With Isabel Barao Ph.D

Dr. Barao is Adjunct Assistant Professor at UNR’s Department of Microbiology and Immunology and Scientific Director of Simmaron Research.

How did you get involved in ME/CFS research?

In 2009, the Whittemore Peterson Institute (WPI) invited me to be their scientific consultant and to find out why NK cells are dysfunctional in CFS. I conducted immunological studies at the WPI until September of 2010.

What has your research into ME/CFS told you about this disease thus far?

Isabel Barao Ph.D

Isabel Barao Ph.D

I believe that variations in particular genes that affect the functioning of the immune system increase the risk of CFS.

You recently presented a paper at the 1st Annual Mountain West CTR-IN meeting suggesting that ME/CFS patients may have higher than normal levels of “hybrid” immune cells. Can you tell us what those immune cells are and what effects they might have?

The ‘hybrid’ lymphocytes are NKT-like cells that are increased in the blood of some of Dr. Peterson’s CFS patients and that may have unique properties in CFS patients.

We are characterizing these immune cells further.

You’re also engaged in a Simmaron Research Foundation study examining genetic changes in a range of immune cells in ME/CFS. Most ME/CFS research has focused on natural killer cells but you’re also really interested in other immune cells. Why?

Because NK cells communicate with B cells, T cells, macrophages, etc. and if the communication between them is defective, immune deregulations involving all these cells can occur and lead to disease. 

What comes next and what are the treatment implications if the study is positive?

Our expectations are that FcRs polymorphisms define CFS and its severity and predict those patients who may benefit from ADCC-based therapies.

Read more about Isabel’s work at Simmaron Research Foundation Study Targeting Roots of Immune System Breakdown in Chronic Fatigue Syndrome (ME/CFS)

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19 Comments

  • DEBRA HANGE

    August 31, 2014 at 7:30 pm - Reply

    OH THANK GOD. I NEED HELP SO BAD.

    • Cort Johnson

      September 1, 2014 at 9:40 pm - Reply

      Hang in there Debra!

      • DEBRA HANGE

        September 2, 2014 at 12:40 am - Reply

        I so hope to get REAL HELP SOON. THANK YOU

  • Simon McGrath

    August 31, 2014 at 7:51 pm - Reply

    Interesting, and always good to see the NIH backing CFS research.
    “Our expectations are that FcRs polymorphisms define CFS and its severity and predict those patients who may benefit from ADCC-based therapies”
    I can see how such defects might lead to problems based with chronic infection, but did Isobel Barao explain why she thinks this is likely to be going on? Eg findings from published or unpublished work?
    Thanks

    • Cort Johnson

      September 1, 2014 at 9:52 pm - Reply

      Hopefully Dr. Barao will chime in. (I presume she has unpublished data) I want to underline, though, how important it is that ME/CFS researchers get into the NIH ‘loop’. The NIH funds most of the medical research in the U.S but getting NIH grants has been very difficult in this field. (NIH funding of ME/CFS is lower, adjusted for inflation, than it was 20 years ago).

      Getting into the NIH ‘loop’ helps, though. One successful grant can often lead to another one – and this one will hopefully lead to a major ROI grant.That’s what grants of this size are designed to do.

      Linking a genetic dysfunction with a different kind of immune dysfunction than has previously been found in NK cells would cement the role the genetics and NK cells in general play in this disorder.

  • Jeff

    September 1, 2014 at 9:43 pm - Reply

    This is really great news. As one of the more consistent findings in ME/CFS is altered and dysregulated immune and especially altered cytokine function, it only makes sense to focus attention on that area. Really impressed with Simmaron Research Foundation – if anyone can find an answer, it would seem to be the great researchers associated with SRF!

    • DEBRA HANGE

      September 2, 2014 at 12:41 am - Reply

      AGREED

  • Dave Downer

    September 2, 2014 at 12:20 am - Reply

    I really believe they are on to something here. Can’t wait for. Outcome as i and so many others are so much suffering.

  • Janice

    September 2, 2014 at 7:26 am - Reply

    Always great news to hear of more research being done

  • Pat

    September 2, 2014 at 6:01 pm - Reply

    “Studies have shown that individuals with genetic alterations (polymorphisms) of the genes associated with that ADCC response have an increased risk of cancer and autoimmune disorders. Genetic impairment of the ADCC response could also make it more difficult to clear herpes viral infections, which are of such interest in ME/CFS.”

    It is so encouraging to see genetic studies going on! I have always believed there is a strong genetic component even though I come from a very large family and, to my knowledge, I am the only one to be diagnosed with ME/CFS and FM, although one niece has been diagnosed with FM but not ME/CFS. My guess is there are probably more but they have gone undiagnosed. There is, however, a large number of various types of cancers and autoimmune diseases in my family, particularly in my generation. My grandparents had seven children and three of those died from cancer. There are 29 first cousins in my generation and, to date, 15 (more than half) of us have had some type of cancer, six of those dying from their cancer. (Those with breast cancer tested negative for the BRAC 1&2 genes.) Fortunately, it appears that cancers are not showing up as much in the next generation, at least yet. There are 79 in the next generation and only three have died of cancer so it would appear that whatever the gene(s) might be, it’s losing its power after my generation. With such a large family history of cancers, I’m stunned that I would be the only one “diagnosed” with ME/CFS.

    Keep studying the genetic and immune dysfunctions. This connection is going to play a major role in the treatment of ME/CFS and probably cancer as well.

  • susan threlkeld

    September 6, 2014 at 12:39 pm - Reply

    I have RH-blood and believe that has something to do with my CFS and pain issues, along with other things like ADD. I believe our genetic makeup is different, and a lot of things go with.Not much is known about this because there has not been much attention to it, if any. This seems to be the common thread in our family. The negative blood not being the only thing different but our entire genetic makeup. I think our immune system is different, our nutritional needs are different, and many other things. Complicated. I’ve been studying this for a long time, and am convinced that this has something to do with my problems and many of my relatives. Anyway, just to point out this genetic difference.

  • James

    September 10, 2014 at 6:52 am - Reply

    How can I become involved in this research please?

  • James

    September 10, 2014 at 6:54 am - Reply

    How can help with this research please?

  • Pam

    September 11, 2014 at 8:53 pm - Reply

    I do not know if there is a connection but a few people in the family (they all lived in different places) had colic as babies, were hyperactive and later developed cfs

  • Annette

    September 22, 2014 at 11:06 am - Reply

    This sounds like great research. Thank you.
    Are any of these genetic polymorphisms covered in 23andme testing?

  • susan threlkeld

    September 23, 2014 at 5:44 pm - Reply

    My son started out hyperactive but now at 36 yrs old he is having fatigue and pain issues, and so is my sister who has had the same issues over the yrs. also my son’s son has started out the same way. I would like to at least be able to help with my grandson with this research. I believe it has something to do with the endrocrine system. Thanks for all who are trying to help with this research.

  • BRENDA M. FLIPPEN

    September 29, 2014 at 7:27 pm - Reply

    Speaking of genetics, I have found 4 cousins who also have FMS/mecfs so far. Just started looking. There are quiet a few of us. This should have been added to my prior inquiry . Sorry,, little foggy today. Thanks for all your research into this,, our lives.

    • susan threlkeld

      September 29, 2014 at 8:31 pm - Reply

      My grandson and son both, would wake up every little while as an infant, and cried a lot. Not sure if it was colic or what. My son would not sleep for a nap at all. He would wake up in 30 min.s. after he went to sleep. My grandson would wake up and cry and would not stop. My son, did at least, sleep at night, I guess… I tell everybody that “I guess he slept, because I was a sleep” That is one time of day that was mine, regardless. But, later on as a toddler, and on up, he had night terrors, (I guess that is what it was) You could set the clock of about an hr. after he went to sleep he would wake up screaming and you could not get him to stop, as a matter of fact, you couldn’t wake him up. The only thing I learned would work, was to put him in the bathtub of water, that would bring him around. Most of the time this happened was if had missed a nap, such as it was, like if we had gone somewhere and he didn’t get to at least rest a few minutes. It was the over stimulation that caused it. Over the yrs he has had a h— of time one way or another. I have planned his funeral many times, especially over the teen yrs. One thing I knew about his funeral was the song that would be sang “go rest high on the mountain” by Vince Gill

  • Sara

    November 15, 2014 at 6:06 am - Reply

    The Open Medicine Foundation is raising money to start the End ME/CFS Project. They have top notch scientist and two Nobel Prize winners including James Watson ( as in Watson and Crick). You can find more information here http://www.openmedicinefoundation.org/

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