Archive for April, 2018

The Autoimmune Virus? Groundbreaking EBV Finding Could Help Explain ME/CFS

Viral Mystery 

“I’ve been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research,” Harley

I sensed some awe in Ron Davis’s voice as he pushed for more understanding of Epstein-Barr Virus’s effects in ME/CFS during a talk at the Brain Science conference.  Davis is not to my knowledge finding much evidence of EBV reactivation in the severe ME/CFS patient study – a surprise – but he is very interested in what happened during that initial EBV infection, which appears to have triggered chronic fatigue syndrome (ME/CFS) in so many people.

Epstein-barr chronic fatigue

A large, complex and very common virus, EBV is responsible for infectious mononucleosis and appears to contribute to numerous autoimmune disorders.

He’s not alone in his “admiration” for the virus. Simmaron’s Advisor, Dr. Daniel Peterson, whose clinical practice and research stemmed from an outbreak in the Lake Tahoe region of Chronic Fatigue Syndrome, has tracked EBV in patients for decades, noting very high titers to EBV and other herpes viruses in subsets of patients.

It’s not surprising that these two important figures have had their eyes on EBV. EBV, after all, is kind of in a league of its own.  An invader of B and epithelial cells, the 50th anniversary of its discovery was recently celebrated with numerous reviews.  Epstein-Barr was discovered in 1966 by Anthony Epstein and Yvonne Barr. It was the first human virus shown to cause cancer. The sequencing of its large genome in 1995 helped launch the genomic era.

One of the more massive and complicated viruses, it’s one of the very few viruses that’s able to avoid elimination: once EBV infects your B-cells, it’s in your body to stay. It’s able to effectively hide from the immune system and reactivate just enough so that when the infected B-cells die it can move on to other cells.

We’re well equipped to ward off EBV when we’re young – it usually produces only minor symptoms – but as our immune systems alter as we age, that changes.  Encountering EBV as an adolescent or adult (infectious mononucleosis, glandular fever)  – as increasingly happens in our germ phobic age – often means months of convalescence as our immune systems struggle to ward off this powerful virus.

The problems don’t stop there. We know that infectious mononucleosis (IM) is a common trigger of ME/CFS but coming down with IM/glandular fever in adolescence has also been shown to increase one’s risk of coming down with multiple sclerosis 2-4 fold and lupus by fifty percent.  Because of EBV’s ability to remain latent in the body, EBV reactivations are a huge problem for transplant patients with compromised immune systems.

The big question concerning EBV is how a virus which has essentially been latent for decades could contribute to serious diseases like MS and lupus. We now may have the answer. Last week, what will probably turn out to be a seminal paper in pathogen research directly showed for the first time how EBV appears to be able to trigger autoimmune diseases later in life and could conceivably play a role in ME/CFS.

The rather hum drum title of the paper “Transcription factors operate across disease loci with EBNA2 implicated in autoimmunity” in the Nature Genetics Journal hardly hinted at the possibilities the paper presents.

Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity John B. HarleyXiaoting ChenMario PujatoDaniel MillerAvery MaddoxCarmy ForneyAlbert F. MagnusenArthur LynchKashish ChetalMasashi YukawaArtem BarskiNathan SalomonisKenneth M. KaufmanLeah C. Kottyan & Matthew T. Weirauch. Nature Genetics (2018) doi:10.1038/s41588-018-0102-3

EBV  consists of several proteins of which EBNA-2 is one. EBNA-2 is EBV’s main viral transactivator; i.e. it’s a transcription factor that turns on genes in an infected cell that help EBV to survive. Essentially EBNA-2 allows EBV to hijack a cell’s genetics and put them to its own use.

The study – produced by researchers at Cinncinnati’s Children Hospital – demonstrated that once EBV infects B-cells, it turns on genes that have been identified as risk factors for a boatload of autoimmune diseases.

It turns out that even though the virus is, so to speak, latent; i.e. it’s not replicating – its transcription factor is still active  – altering the expression of our genes. The genes that it affects just happen to be the same genes that increase the risk of developing lupus, multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes.  Apparently decades of genetic assault from EBV’s transcription factor can set the stage or at least contribute to many autoimmune diseases.

Chronic diseases are usually caused by a variety of genetic and environmental factors. Because not everyone with these transcription factors comes down with a chronic illness, other factors must play a role. The authors believe, though, that the gene expression changes induced by the virus in the B cells could account for a large number of people with lupus and MS who fall ill.

“In lupus and MS, for example, the virus could account for a large percentage of those cases. We do not have a sense of the proportion in which the virus could be important in the other EBNA2-associated diseases,” Harley

Chronic Fatigue Syndrome and EBV/Infectious Mononucleosis – A Short History

Researchers have been trying to figure out – mostly unsuccessfully- what the heck happens to plunge people with infectious mononucleosis into ME/CFS for quite some time.

trigger

Infectious mononucleosis/glandular fever is believed to be a common trigger of ME/CFS

In fact, infectious mononucleosis/glandular fever was probably the first disease associated with ME/CFS. Studies in the mid-1990’s, including one from the CDC, suggested ME/CFS was, at least in part,  “chronic infectious mononucleosis” or “chronic mononucleosis syndrome“.  Even Stephen Straus penned a paper on the “The chronic mononucleosis syndrome“.

Straus’s small 1989 study reporting high rates of psychiatric diagnoses in ME/CFS patients prior to their becoming ill set a theme in motion which was disproved by two Peter White  ME/CFS IM publications.  White found IM/glandular fever to be a particularly strong trigger of ME/CFS which he concluded was probably responsible for about 3,000 new cases of ME/CFS a year in the U.K.

A 1992 Swedish study began a trend of examining people with ME/CFS during infectious mononucleosis and afterwards in order to try and determine what happened. That study concluded that whatever happened was not due to EBV reactivation.

In 2010 Taylor found reduced peak oxygen consumption during exercise in adolescents with ME/CFS after IM compared to IM patients who had recovered. Broderick’s finding of altered cytokine networks associated with Th17 in ME/CFS patients following IM suggested immune dysregulation had occurred.

Glaser’s 2005 study suggested that an EBV encoded enzyme produced by a non-replicating form of EBV could be producing symptoms in ME/CFS.  Lerner’s 2012 study suggested that antibodies to two EBV produced proteins were commonly present in ME/CFS – suggesting that a prolonged immune reaction to EBV might be occurring in ME/CFS as well.

In 2014 Loebel/Scheibenbogen suggested that ME/CFS patients may be having difficulty controlling the early stages of EBV reactivation.   Loebel’s 2017 follow up study suggested that ME/CFS patients’ immune system might be over-reacting to an EBV produced protein and that autoimmunity might be involved.

Leonard Jason’s large IM college student study will hopefully provide clues why some people never recover from it. He’s completing data analysis of a study examining college students who came down with infectious mononucleosis and then ME/CFS. So far Jason has found that at least 4-5% of college students come down with IM while at school.

Treatment Implications

Interestingly, several drugs that are available can block some of the transcription factors EBV has inserted into B-cells.  (I was unable to determine what they are.) The authors also hope the study will help spur more efforts to produce an EBV vaccine.

Next For ME/CFS and EBV

Now that we have evidence that EBV/IM contributes to many autoimmune diseases, it’s hard to think that ME/CFS is not somehow involved. Chronic fatigue syndrome is different in that infectious mononucleosis (and other infections) immediately triggers ME/CFS in many people. What we don’t know is if bouts of IM also trigger ME/CFS 5, 10, 15 or more years later as occurs in these other disorders.

Opportunities for Collaboration Open Up

The big question awaiting ME/CFS now is if the abnormal transcription factors associated with the autoimmune diseases in the recent paper are present. The good news is that a study determining that appears to be within reach of an ME/CFS researcher with the technical ability and funds. In an unusual move, the Cincinnati researchers are making the computer code they used available to other researchers.

“We are going to great lengths to not only make the computer code available, but all of the data and all of the results. We think it’s an interesting approach that could have implications for many diseases, so we’re contacting experts on the various diseases and sharing the results and seeing if they want to collaborate to follow-up on them.” Weinrauch

“This discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders” Harley

Collaboration

The Cinncinnati team is providing its computer code free to other researchers

They believe EBV will be implicated in many more diseases, and there is already some evidence that it is.  Using the same analytical techniques, they’ve already identified 94 other diseases including many non-autoimmune diseases in which EBV may play a role.

This is one of the few studies in which the researchers are so jazzed by their results that they’ve dropped all pretenses to modesty. The study results need to be validated, but because EBV is so common and is potentially linked to so many autoimmune (and other diseases), it has the potential to rewrite our understanding of how autoimmune diseases arise. The authors fully recognize the potential importance of their finding. The lead author of the study, John Harley, said:

“I’ve been a co-author in almost 500 papers. This one is more important than all of the rest put together. It is a capstone to a career in medical research,” Harley

One of the senior authors of the study stated:

“This same cast of characters is a villain in multiple immune-related diseases. They’re playing that role through different ways, and doing it at different places in your genome, but it’s the same sinister characters. So if we could develop therapies to stop them from doing this, then it would help multiple diseases.” Matthew Weirauch

 

POTS Rising! Research & Advocacy Producing Breakthroughs in Neglected Disease

April 28, 2018

Remarkable Progress

It’s rare that a clear cause of disease like postural orthostatic tachycardia (POTS) or chronic fatigue syndrome (ME/CFS) or fibromyalgia (FM) shows up, but that appears to be what’s happening in POTS.

focus - POTS

Researchers are increasingly focusing on autoimmune aspects of POTS

The progress is all the more notable in POTS given the newness of the disease.  The name was only coined in 1993 and the disease still lacks a dedicated funding stream at the NIH (but see below). Nor does the NIH track POTS funding the way it does other diseases.  It was only recently that the World Health Organization created an ICD code specifically for POTS. While the disease is mostly an afterthought at the NIH, it affects a large number of people (1-3 million in U.S.)

Despite its humble beginnings remarkable progress in understanding the disease is being made.  That’s good news for people with ME/CFS given the high incidence of POTS (11-40%) in the disease. Plus it shows that even a small research community can make significant strides in a disease if they target the right area.

Autoimmune Disorder

With its female dominance and often an infectious trigger, POTS, like ME/CFS, has always been a candidate for classification as an autoimmune disease.  In fact, autoimmunity has been showing up in orthostatic intolerance in general lately. Plus it’s shown up in an array of cardiovascular diseases including hypertension, cardiomyopathy, myocarditis and cardiac arrhythmias, each of which can cause problems standing.

Orthostatic Hypotension

It turns out there are many ways to mess with our circulatory systems.  A University of Oklahoma group has been driving the findings in mostly small studies. In 2012 that group reported that people with orthostatic hypotension, who experience severe drops in blood pressure while standing, commonly had autoantibodies to the receptors on the outside of cells that regulate autonomic nervous system activity. Remarkably, autoantibodies  were found in no less than 75% of the study participants.

The adrenergic (B1AR, B2AR) and muscarinic (M2R, M3R) receptors identified affected blood flow across the body. Different symptoms appear to result depending on which receptor is involved.

People with severe blood pressure drops within a few minutes of standing, for instance, tended to harbor B2AR and M3R autoantibodies which affect the vasodilation of our blood vessels. Because our blood vessels constrict or narrow when we stand in order to halt the gravitational flow of blood to our limbs, vasodilation during standing is exactly the wrong strategy.

Other people with dramatic heart rate increases while standing tended to harbor M2R and/or β1AR autoantibodies.

POTS

In 2014 the Oklahoma group’s study in the Journal of American Heart Association found evidence of three autoantibodies in POTS. This time the Oklahoma group predicted they would find autoantibodies to a receptor (α1 adrenergic receptor – α1AR) that causes our blood vessels to contract.

They found that, but in a twist, they also found additional autoantibodies: to the β1AR receptor in all the POTS patients, and vasodilatory autoantibodies to the β2AR receptor in half of them. They believe that these autoantibodies enhance norepinephrine’s effect on the heart; i.e. they increase the heart rate problems in POTS.

Autoimmunity POTS

Autoimmune processes that affect the blood vessels may define disorders that produce problems with standing.

They posit, interestingly, that problems with blood pressure not heart rate increases are the primary problem in POTS. They believe that when POTS patients stand, their α1AR autoantibodies smack the αIAR receptors, causing problems with blood vessel contraction. That allows blood to drain from POTS patients’ brains into their lower bodies causing fatigue, dizziness, etc. In order to compensate, they jack up their sympathetic nervous system activity with norepinephrine in order to maintain blood pressure.

Unfortunately, since POTS patients also harbor autoantibodies which cause them to increase their heart rates, the result is sometimes astonishingly high heart rates while standing. Since a heart beating too fast has the same effect as a heart beating too low (reduced blood flow), the ploy doesn’t work and POTS patients experience dizziness, fatigue, etc. upon standing.

In effect the POTS patients struck out on two levels; not only did they have autoantibodies that might be imperiling their ability to maintain their blood pressure while standing, they also had autoantibodies that dramatically increased their heart rates.

New Study – New Autoantibody

In a follow up 2018 study published in the Journal of the American Heart Association, the group looked at an entirely different type of autoantibody – the angiotensin II type 1 receptor (AT1R) that regulates blood pressure via the renin-aldosterone system. The renin-aldosterone system also regulates blood volume, which is often low in ME/CFS.

The study was again small (17 POTS patients) plus 16 controls, but once again the results were highly significant with 12/17 POTS patients but none of the controls exhibiting autoantibodies to AT1R. Plus all the POTS patients also had autoantibodies to either or both of the AT1R and the α1‐adrenergic receptor.

Because the renin-angiotensin-aldosterone system works more slowly than the aforementioned responses, it appears that many POTS patients may suffer from both a rapid and a more prolonged dysregulation of their circulatory systems.  When placed in a rabbit model, the ATIR autoantibody effectively duplicated the effects of the α1AR autoantibody – it stopped the blood vessels from constricting properly, again resulting in blood pooling in the lower extremities – and in humans feelings of fatigue, dizziness, etc.

In a nice fit, several POTS studies have documented problems with the renin-angiotension-aldosterone system, which could be caused by autoantibodies like ATIR. One study, which found elevated Ang II levels and low aldosterone levels, suggested that receptor problems were interfering with transformation of Ang II to aldosterone. The authors of this study suggested that the autoantibody found could indeed be the missing link.

Another Autoantibody (!)

We’re still not done with autoantibodies in POTS. A recent presentation which found a fourth autoantibody (to the M1 receptor) suggested POTS patients may be swimming in autoantibodies which negatively affect their circulatory systems.

Spectrum Disorder?

These investigators believe POTS is part of a spectrum of diseases (OH, POTS, cardiovascular diseases, (ME/CFS?)), all of which harbor autoantibodies that interfere with blood vessel contraction/dilation and the heart rate.

Dysautonomia International – Moving Forward on POTS

Since being co-founded in 2012 by Lauren Stiles, Dysautonomia International has grown rapidly and is now providing substantial funding for POTS research. A very dynamic organization, I was glad to have the opportunity to ask its President about its POTS work, where we are on autoimmunity and POTS, and DI’s recent advocacy work.

What kind of POTS funding has Dysautonomia International provided? 

Dysautonomia International

Dysautonomia International has grown rapidly in just five years.

Dysautonomia International has funded over $300,000 in POTS Research Fund grants to support the work of Dr. David Kem and colleagues at University of Oklahoma, exploring the role of autoimmunity in POTS, seeking to identify diagnostic biomarkers, and eventually the development of targeted immune therapies. Dr. Kem’s recent publication documenting the presence of angiotensin receptor antibodies in POTS was one of several important publications that resulted from these grants, and there are additional autoimmune POTS related studies still in progress at the University of Oklahoma. We have also funded autoimmune POTS related studies at Mayo Clinic and University of Texas Southwestern, which are in progress.

How far are we from establishing that at least a major subset of POTS patients have an autoimmune disease?

Most POTS experts acknowledge that a subset of POTS patients have an autoimmune problem. Defining what percentage of patients that is depends on how we define what we mean by “an autoimmune problem.”

For example, the largest cohort study on POTS to date with over 4,000 patients enrolled (lead by Dysautonomia International, Vanderbilt University and University of Calgary), found that 16% of POTS patients report being diagnosed with a known autoimmune disease, most often Hashimoto’s, Sjogren’s, lupus and celiac.

Then there is a larger group of POTS patients who have positive blood tests on common antibody tests, such as TPO, ANA or SS-A, but they don’t meet the criteria for a known autoimmune disease.

POTS patients have signs of an autoimmune disease but larger studies are needed to validate them.

Then we have several small cohort studies, usually 40 patients or less, showing that nearly all POTS patients have antibodies to various cell surface receptors that play a role in regulating the autonomic nervous system (adrenergic, muscarinic and angiotensin antibodies).

This last category of antibodies are also present in other medical conditions, several of which are associated with autonomic dysfunction, such as orthostatic hypotension, Sjogren’s syndrome, Chagas disease, dilated cardiomyopathy, and ME/CFS.

We need a lot of additional research before we can go from “we found these interesting antibodies that might play a role in POTS” to “we’re sure POTS is an autoimmune disease,” but that research is happening at several universities. The antibody tests are being refined. The small cohort studies are being repeated on larger cohorts. Researchers are starting to look at immune modulating treatments too.

I’m proud to say that Dysautonomia International is very much part of this effort, not only funding many of the studies, but also facilitating the larger cohort studies at our annual conferences, and connecting researchers who should be talking to each other together.

The NIH didn’t have a dedicated funding platform for POTS research but now things are looking up. What happened?

After Dysautonomia International’s July 2017 Lobby Day and our first Congressional Briefing on POTS in October 2017, Congress adopted our requested language directing the NIH to “stimulate the field’ of POTS research and “develop strategies that will increase our understanding of POTS and lead to effective treatments.” We’re continuing to meet with NIH to see what this will lead to in 2018, which we hope will be NIH’s first POTS specific call for proposals. Find additional details on our blog.

Conclusion

The POTS autoimmune finding are helpful for ME/CFS in several ways.  For one they show that researchers even in greatly underfunded diseases can make substantial progress if they target the right area. Secondly they’re beginning to demonstrate a strong autoimmune basis for a disease which produces similar symptoms to ME/CFS and which has a substantial overlap with it. Finally some of the same autoantibodies (and other ones) have been found in ME/CFS and interest in ME/CFS as an autoimmune disorder is picking up.  A recent review paper presented evidence that at least a subset of ME/CFS patients have an autoimmune disease. That will be covered in a future blog.

Hope for an ME/CFS Autoimmune Subset: A German Researcher Steps Forward

German Researcher Steps Up

Carmen Scheibenbogen MD is another sign that the ME/CFS field is slowly but surely hopefully catching on. Scheibenbogen is relatively new to this field, but she’s not new to medical research. A trained oncologist and hematologist as well as a physician and Professor of Immunology in Berlin, her research resume includes over 150 publications dating back 25 years.

scheibenbogen

Dr Scheibenbogen has identified what she believes is an autoimmune subset in ME/CFS. (Image from Invest in ME)

In short, she’s a respected and established researcher, and one from Germany to boot. (I can’t remember the last German researcher to take on ME/CFS.) Her path to ME/CFS has not been an easy one. Germany hardly acknowledges ME/CFS as a disease, and doesn’t fund ME/CFS research – if I’m reading her right, there is apparently literally no avenue to apply for ME/CFS research funding there.

Yet she’s very quickly become one of our most prolific researchers. Over the past four years her team has published no less than seven papers, has won two Ramsay Awards, and played a central role in the development of the new European Research collaboration, EUROMENE. Her biosketch lists CFS/ME, Immunodeficiency, and Cancer Immunology as her main research interests.

Scheibenbogen’s first ME/CFS publication In 2014 found ME/CFS patients mounting a feeble response to Epstein-Barr virus (EBV) . The reduced response to EBV reactivation could help explain the ups and downs seen, particularly during stressful situations.

In 2016, figuring that when Rituximab worked in ME/CFS it probably did so by whacking antibody producing B-cells, her group examined antibodies against a variety of receptors that affect blood flow, the autonomic nervous system, etc. They found that about 30% of ME/CFS patients in a large study (n=293) had increased levels of antibodies to adrenergic (B2) and/or muscarinic M3/M4 acetylcholine receptors (M3/M4).

That suggested that the immune systems of a significant subset of ME/CFS patients might be attacking the receptors on cells which regulate blood flow, lung functioning, muscle contractions and attention. Furthermore, the finding (a “remarkable” one they said) that the antibody levels of two receptors correlated with a host of immune factors (immunoglobulin levels, T cell activation, elevated ANA, TPO antibodies) suggested that this subset of ME/CFS patients are suffering from an autoimmune disease. Scheibenbogen has suggested that the kind of ME/CFS you have may be dependent on the kind of autoantibodies present in your system.

See Bad Bacteria, Brainstem Abnormalities and Progress with Rituximab: the Invest in ME Conference

Similar antibody findings have been found in a range of diseases (postural tachycardia, regional pain syndrome, Alzheimer’s, Sjogren’s syndrome, asthma) some of which have been associated with ME/CFS.

They also noted that immunoadsorption factors that are able to mop up these antibodies had proven to be helpful in some diseases. Two years later they put that idea to the test.

Possible Autoimmune Treatment

PLoS One. 2018 Mar 15;13(3):e0193672. doi: 10.1371/journal.pone.0193672. eCollection 2018.
Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME.Scheibenbogen C1,2, Loebel M1, Freitag H1, Krueger A3, Bauer S1, Antelmann M1, Doehner W4, Scherbakov N4, Heidecke H5, Reinke P2,3, Volk HD1,2, Grabowski P1.

Adsorption

Adsorption vs absorption – By Daniele Pugliesi – File:Absorbimento e adsorbimento.svg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20486772

They used a blood purification technique called immunoadsorption to eliminate the B2 antibodies from people with ME/CFS who’d had a post-infectious onset and high B2 antibody levels. Immunoadsorption (IA) was given five times over seven days to completely wash out the antibodies. Over the next six months the participants’ symptoms, muscle strength, endothelial functioning and immune factors were watched.

Findings

Significant improvement eventually followed by a relapse was the order of the day. One patient who could barely walk prior to the treatment was able to walk several hundred yards at the end of the IA process. She completely recovered for seven weeks and then relapsed. Another patient improved enough to go back to work but then relapsed. Five patients who improved started to relapse by the end of the six months. Three patients – a good third of the study – felt significant improvements in fatigue lasting at least 12 months.

The levels of all four antibodies (B1, B2, M3 and M4) declined after the treatment in all 9 participants. These are good results which are hampered by the small sample size and lack of a placebo control. Through our experiences with Rituximab, Synergy and Mirogabalin we’ve learned how little to trust early results.  Still, research has to start somewhere and the results thus far present hope for a significant subset of ME/CFS patients.

Present and Future Work

Ramsay Award Standout

The Solve ME/CFS Initiative (SMCI) provides funding to five or so researchers every year in its Ramsay Awards. The Awards are quite competitive with SMCI receiving far more applications than it can fund, but over the past two years the Scheibenbogen group has won two – the only group to do so.

2016 Award

Citing “ample evidence of an autoimmune pathomechanism” the Scheibenbogen team will be digging into the genetics of their “autoimmune subset”. They’ll be determining if genetic abnormalities in the enzymes or transcription factor that turn on the autoimmune processes are present. They’re also analyzing the immune cells (dendritic cells, regulatory B-cells) known to produce autoimmune responses.

This is one of the first times that I’m aware of that a research group has targeted a subset and dug deeper into it.  Scheibenbogen’s focus is clearly good news for people in that subset but it’s also good news for people outside of it. If she’s found a robust subset then it needs to be peeled off from other ME/CFS patients because it’s undoubtedly confounding study results for those patients.

2017 Award

The 2017 Ramsay Award will determine if T-cells and monocytes are up to the task in ME/CFS. We know that NK and probably T-cells are laggards in ME/CFS patients’ immune systems, but other immune cells are largely untested.

Following on recent findings of impairments in energy production, the Scheibenbogen group is going to determine if T-cells and monocytes have the energy to spring into action when needed. Immune cells are mostly quiescent until they come across a pathogen, at which point they’re required to rev up their engines and explode into action. If they don’t have the energy to “explode” they’ll have difficulty fighting off bugs.

If I have it right, they’re also going to stimulate cells using adrenergic and acetylcholinergic factors to see if they affect their metabolism or energy production. Given the role these factors appear to play in the deranged stress response found in ME/CFS, finding a metabolic tie-in would be exciting indeed.

Simmaron Scheibenbogen Collaboration Underway

The Simmaron Research Foundation is also working with Dr. Scheibenbogen to identify the subset of Dr. Peterson’s patients who fit the autoimmune profile, and to further characterize the subset from a clinical perspective.

A Leader

Over the past five years Scheibenbogen has become deeply immersed in ME/CFS. She was the lead author of a paper on the EUROMENE network, which contains researchers and clinicians from 17 European countries. Euromene was accepted into the COST (Cooperation in Science and Technology) framework which was established by the European Union to support collaboration in scientific endeavors. While COST does not fund research studies, it does fund networks and provides networking possibilities across the European Union.

EUROMENE members

EUROMENE members

One goal of Euromene COST Action is to establish a “sustainable integrated network of researchers in Europe working in the field of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and to promote cooperation between research groups.

Coordination and collaboration appears to be becoming a bigger and bigger theme. The OMF and the SMCI held collaborative and networking meetings last year. The NIH research centers are collaborating on one large project. Canada’s May Montreal conference is focusing on establishing cooperative efforts to understand ME/CFS. (Dr. Scheibenbogen will be attending.) The OMF’s next conference is set for September of this year.

However Dr. Scheibenbogen got interested in ME/CFS, it’s great to see her get so involved so quickly. She reminds me of another relatively new researcher in the field – Dr. Maureen Hanson – who quickly cranked out research studies and is now leading an NIH ME/CFS research center. It’s good to see new researchers have success in this field.

Of course, the going is still tough. In an SMCI interview Dr. Scheibenbogen seemed astonished at the lack of opportunities for research into what she described as a frequent and severe disease.

But still the situation is very disappointing with so little support for patients and research and almost no interest from pharmaceutical companies to perform clinical studies. I am a trained oncologist and hematologist and there the situation is so different with so much research and drug development.

Like everyone else in this field, Dr. Scheibenbogen is a pioneer and pioneers by definition have rough going. Like the pioneers of old she’s forging a path through some hostile territory, not as the pioneers did in the old West but this time German medical circles.  Her work is getting results, though, results that her colleagues will surely notice.  Here’s to a new presence in the field who’s put, perhaps for the first time, Germany – the most powerful nation in Europe – on the ME/CFS map.