The Symposium on Viruses in Chronic Fatigue Syndrome (ME/CFS) (June 2008): Part II by Cort Johnson
A Neuro-Immune Fatigue Subset?
D. Peterson. Antiviral treatment of patients with HHV-6, EBV and enterovirus: case reports
There’s this 15-30% percent number floating around ME/CFS. Several doctors have spoken of the 20% of patients who seem immune to their approach. There’s about 20-25% dropout rate in behavioral studies. There’s the 25% ME group of really disabled patients.
Then there’s Dr. Peterson 15-20% group. This is a group for whom the standard toolbox doesn’t fit; they don’t respond to supplements or the commonly used drugs and behavioral modification has no effect. Dr. Peterson thinks they have a different kind of disease altogether. He calls them the neuro-immune fatigue group.
These patients generally have headaches, cognitive problems, paresthesias (pins and needles feelings), autonomic dysfunction (presumably increased heart rate, trouble standing, etc.), abnormal MRI reading and SPECT scans. Cerebral spinal fluid (CSF) studies indicate increased total protein, myelin basic protein, lactic acid, lymphocytes and opening pressure.
They have active viral infections usually with cytomegaloviruses, HHV-6, Epstein-Barr virus (EBV), a gamma herpes virus and enteroviruses. Their gene expression, cytokine and protein expression results suggest their immune systems are chronically activated – as one would expect.
The antiviral drugs Dr. Peterson uses to treat these patients include Foscavir, Valcyte, Cytovene, Zovirax, Valtrex, Vistide and Ampligen (approved for use in Canada).
A Cancer Subset? Dr. Peterson reported that a subset of his patients with chronic HHV-6 infection exhibit a kind of process – called T-cell receptor gene re-arrangement – that’s usually found only in lymphoma patients. This process apparently increases the risk of T-cell becoming cancerous. The Whittemore-Peterson Institute is reportedly focusing on this subset of patients.
Dr. Peterson’s work, if substantiated, underscores how important subsets may be in this disease and how incredibly damaging researchers inability to ferret them out has been. A twenty percent subset in a disease will do two things; it will make it difficult to find consistent findings for the other 80% of the patients and make it almost impossible to detect the subset itself If Dr. Peterson’s subset is a truly different kind of patient the 20% subset represents an ongoing tragedy. (One study of the longterm effects of ME/CFS did not find increased mortality in the disease).
Dr. Peterson’s work, too – despite his years of experience – must be also regarded as ‘preliminary’ as is any unpublished work. In order to truly impact the course of ME/CFS research must be published and replicated – hopefully by different researchers. The word is, though, that Dr. Peterson, a busy physician will, with the help of Judy Mikovitz, the new Director of Research at the Whittemore-Peterson Institute (WPI) will be publishing shortly.
Dig Deeper: the Whittemore Peterson Institute Comes Out of the Closet / The Whittemore-Peterson Institute
Antiviral Drugs – Hope on the Horizon?
Prichard, New Developments in therapies for HHV-6 Infection
‘Precious few molecules with good activity against HHV-6 have been identified and none have been approved.” M. Prichard
Dr. Prichard noted we have a long way to find a really good drug against HHV-6. One problem with the current batch is dose-related toxicity. At high enough doses they can indeed kill the bugs but at the risk of injuring or killing the patient. Dr. Prichards presentation suggested that the next round of antiviral drugs will be more effective and less toxic.
In Development
Artesunate – Artesunate is a well tolerated drug approved for malaria (in Europe) that possess antiviral activity as well. In vitro (lab) studies found it was highly effective against one of HHV-6’s cousins; the cytomegalovirus.
An HHV-6 Foundation funded study indicates artesunate also effectively inhibits HHV-6A in the lab. This drug is particularly promising because, in contrast to ganciclovir and foscarnet, it hits HHV-6 early in its life cycle. If HHV-6 produces a kind of smoldering infection that alters cell functioning in ME/CFS and other diseases then hitting it early will be critical. What a boost it would be to find an already approved drug that was effective against HHV-6.
Cycloprovir – analogue of ganciclovir but potentially much more effective against HHV-6. (Valcyte converts to ganciclovir in the body. Ganciclovir interferes with viral replication.
CMX001 – a variant of Cidofovir – is highly effective again many DNA viruses and is 3x’s better than Cidofovir against all herpes viruses in the lab. Its antiviral activity in animal models is very good as well. In the first clinical study it was well tolerated.
CMV423 – a new compound very effective against HHV-6 and cytomegalovirus
HPMP-5-azal – Six times more effective against HHV-6 than Cidofovir. Much more efficient and much less of the drug is needed. This is important because toxicity is a big problem with cfidovir. Possibly a big hit.
Marabavir (MBV) – inhibits cytomegalovirus replication. Currently in Phase III trials. Good against EBV. Contrary to previous reports, possibly good against HHV-6. About 50-100 times more efficient than cidofovir in some tests.
Arysulfone derivatives – good antiviral activity, among most potent of anti-virals.
Valomaciclovir and foscarnet-AZT and HHV-6. K. Yao.
Laboratory studies suggest that using Valomaciclovir and foscarnet-ZT in combination resulted in greater than 90% suppression of HHV-6 after three days. This drug is also being tested in a clinical trial at the University of Minneappolis to treat EBV mononucleosis.
Report From the Bench: An ME/CFS Physician on Antiviral Treatments in Chronic Fatigue Syndrome (ME/CFS)
K. De Meirleir Antiviral Treatment Strategies in Chronic Fatigue Syndrome
“Today using combinations of immunomodulators, antivirals, nutriceuticals and antibiotics we are able to obtain an acceptable clinical results in 70% of CFS patients.”
Dr. De Meirleir has treated 1000’s of ME/CFS patents. He pointed out how little hard data there was on the efficacy of anti-viral treatments in the disease.
Antiviral Treatments
Immunoglobulins – could benefit ME/CFS patients by neutralizing viral antigens and by rebalancing the immune system. They’ve had mixed results in placebo-controlled studies. One study on adolescents suggested they can be very effective. He used low doses of IgG1 or IgG3.
Dig Deeper! IVIG in chronic fatigue syndrome (ME/CFS)
Antivirals – Again we hear the big problem with using antivirals is diagnosis. Physicians need solid and reliable viral markers to determine which patients antivirals will be effective with. Until they can get them they’ll continue to use broad spectrum antivirals and immuno-modulators that may or may not be effective against a particular pathogen.
Dig Deeper! The Antivirals in Chronic Fatigue Syndrome (ME/CFS)
Ampligen – physicians using the drug now have 20 years of experience with it. He noted that two double-blinded, placebo-controlled and two open label studies have found increased cognitive functioning and exercise capacity. Ampligen may be particularly effective in post-EBV cases of ME/CFS.
Kutapressin (Nexavir) – in test tubes Kutapressin (now called Nexavir) inhibits EBV replication and blocks EBV from infecting macrophages. Anecdotal activity suggests that Kutapressin works. Dr. Enlander has unpublished data indicating that 63% of ME/CFS patients ‘respond’ to a brand of Kutapressin he uses called Hepapressin + B-12. Dr. De Meirleir found that 70% of his patients responded quite well to Nexavir (20+ increase in Karnofsky scale in 6 months. This is about double the increase Dr. Cheney’s patients showed on porcine cell factors).
Dig Deeper! Nexavir (Kutapressin in Chronic Fatigue Syndrome (ME/CFS)
Aciclovir – no beneficial effects found over placebo. No positive immunological effects.
Amantadine – inhibits viral infection of the cell and increases dopaminergic activity in the brain. Amantadine has been used to relieve fatigue in MS patients for years. Dr. De Meirleir said it does relieve fatigue in CFS patients as well but a cross-over study found no significant benefit and increased numbers of side effects.
Dig Deeper! Amantadine in chronic fatigue syndrome (ME/CFS)
Thymalfasin (Zadaxin) – new drug used in Italy and Asia to fight chronic hepatitis C. Excellent results reported in off-label uses on chronic fatigue syndrome (ME/CFS) patients in Europe. A placebo-controlled trial is planned.
Azithromycin – an antibiotic that appears to have antiviral properties and is able to penetrate the blood-brain barrier, an important consideration with central nervous system infections. One study reported 50% response rate in ME/CFS. His and Dr. Nicholson’s findings in the US are similar.
Dig Deeper! Azithromycin in chronic fatigue syndrome (ME/CFS)
The Future – is about using new tools such as gene and protein expression and better viral diagnosis protocols to put ME/CFS patients in the correct subset and then targeting the right (new) antivirals and other therapies at them.
(This might not be as difficult as it sounds. If gene and protein expression technologies can just find these subsets then the rest, at least so far as I understand, might be fairly cheap and easy. From what I’ve heard it’s not expensive or particularly difficult to test for a single or couple of upregulated genes – the key is finding them. )
(The gene expression news right now is ‘pretty good’. Dr. Kerr was able to replicate his former results – a big step forward – and it seems like almost every major group – from the CDC to the Whittemore-Peterson Institute to the Montoya studies to the NIH – is taking a hard look at them. Dr. Kerr believes he has found some subsets but it’s not clear yet how ‘tight’ they are.
(Gene expression studies are not at the point, though, where they can identify, say, a central nervous system HHV-6 subset. Dr. Kerr’s repeated identification of high levels of activity in a gene known to be upregulated during Epstein-Barr Virus infection suggests he could be beginning to open up a viral reactivation subset. The Dubbo gene expression studies, on the other hand, found few meaningful correlations in their gene expression studies of their acute onset post- infectious chronic fatigue syndrome (ME/CFS) and Dr. Lloyd does not believe they will play a major role.)
(One key to improving gene expression’s efficacy may be doing complex analyses that combine clinical, laboratory and gene expression data together to ferret out specific sets of patients. This was tried in 2006 in the Pharmocogenomics projects to quite mixed results. The winner of the CAMDA competition that used the same dataset did, however, use complex multidimensional analyses to pick out a gene (FORKHEAD BOX gene) that was associated with immune depletion. Perhaps in the absence of reliable pathogen data these complex multi-variate analyses will eventually be able to pick out pathogen (and other) subsets.
(The FORKHEAD BOX study was one of the most tantalizing studies to come out of the Pharmocogenomic’s study effort. One wonders if, with the financial hit the CDC’s CFS research program has taken funding wise, if it was just left on the shelf.)
(If researchers can find key indicators across a variety of tests they should be able to formulate an algorhythm that could be cheaply tested for. Such an algorhythm could be something like ‘Subset A” = low cortisol plus X, Y, Z upregulated genes plus D and C parameters. These studies are expensive and will require a boost in federal funding for them to come to fruition. )
Dubbo: Not Dead At All
Andrew Lloyd. Investigation of the pathogenesis of post-infective fatigue in the Dubbo infection outcomes study (DIOS)
Dubbo (pronounced ‘duh-bow’ not ‘dew-bow’) has had its troubles lately. When funding for the CDC’s CFS research team tanked they were cast adrift. Attempts to get several NIH Neuroimmune CFS Grants inexplicably failed leaving them in even deeper waters. One wondered if the Dubbo’s projects time – once one of the shining lights of ME/CFS research – was over. Somehow, though, they’ve managed to keep going. 
The Dubbo study’s finding haven’t exactly lit the ME/CFS world on fire either. Dr Lloyd’s rather categorical announcement that neither infectious activity nor immune over activation was driving this illness didn’t endear him to a good number of researchers. It didn’t help that the Dubbo studies have found more about what chronic fatigue syndrome is not than what is; thus far their results have suggested ME/CFS is not due to an inability to fight off the infection or an over-active or under-active immune response.
Dr. Lloyd’s recent statement that based on his findings he believes the jury is still out as to whether gene expression will tell us anything about this disease was probably not eagerly greeted in many quarters. One began to wonder if the Dubbo study was ever going to announce anything positive at all about this disease.
Dig Deeper: the Dubbo studies in review
A Remarkable Unanimity. But the Dubbo studies are back and in a big way. The data from all the pathogen cohorts (EBV, Ross-River and Q-fever) have now been analyzed and they all show a remarkable unanimity. In each of the cohorts the acute symptoms (fever, sore throat, etc.) fade leaving behind a fatigue, muscle and joint pains and, in some, mood disorders.
The rate of post-infectious fatigue or ME/CFS is almost identical at 12 months (6%) and 24 months (3%) among the three cohorts. The key findings of the early studies were repeated in each of the other pathogen cohorts. It turned out the prior findings weren’t a case of concentrating on the wrong pathogen (EBV) as some have suggested; these appear to be standard outcomes for acute onset ME/CFS patients.
Different Pathogens / Different Patients = Same Disease: Consider how different these pathogens are to get a sense of how remarkable these findings are; the Epstein-Barr Virus strikes younger people, the Ross River Virus hits middle-aged people and Coxiella burnetii stricks only middle-aged males in the farm community. Two are viruses and one is a bacteria and they all produce different symptoms in the beginning but all produce not only the same kind of ME/CFS but they produce the same rates of ME/CFS a remarkable finding!
Until the latest study (see below) the only abnormality the Dubbo groups been able to distinguish was that the patients who stayed ill got whacked hard early in their illness. Dr. Vollmer-Conna explained that the initial illness severity was not a trivial factor; it was in fact a surprisingly strong indicator of who was going to stay ill. It also appeared to predict duration as well; the people who got really sick early on generally stayed sicker longer.
Still this wasn’t much – it was after all just a self-reported symptom – not exactly the kind of fact that could turn the scientific world on its head. It did suggest, though, that the problem in chronic fatigue syndrome (ME/CFS) occurred very early – during that period when the patients had little idea they were fighting off anything more than another cold and certainly long before they could begin to guess their lives were being perhaps irrevocably altered. The next phase of Dubbo studies may have uncovered a piece of what happened.
Breakthrough in Dubbo?
Uté Vollmer-Conna. Cytokines in post-infective fatigue. 
Dr. Vollmer-Conna started off her talk by noting how disappointing the cytokine findings thus far had been. Cytokines – immune agents that travel through the blood turning on immune cells when the body is fighting off infection – produce the ‘sickness response’ that makes us so miserable when we are ill. The infectious onset and similar symptoms seen in ME/CFS seemed to make cytokines the perfect fit for this disease but thus far the Dubbo studies had found no evidence that cytokine levels were increased as the disease progressed.
Armed with evidence suggesting the early stages of the disease were the most important they took a close look at the early cytokine data. They found that the people with the severest symptoms (i.e. the soon to be ME/CFS patients) had the highest levels of cytokines, but perplexingly this was only true in the acute illness and not later in the ME/CFS phase.
An Illness Begins Unraveling? This suggested that the chronic fatigue syndrome (ME/CFS) patients had a tendency to pump out more cytokines than normal early in an infection. Next they asked why. They found the ME/CFS patients had very significantly increased risks of carrying two variants of genes that could increase their symptoms during illness. (Different types of a single gene (a polymorphism) are common in population. Typically these variants tend to code for stronger or weaker gene activity).
One of these gene variants coded for increased pro-inflammatory cytokine activity; the other for decreased anti-inflammatory activity. Having either by itself significantly increased the risk of illness but the risks were increased considerably more in people who carried both of them – these were pretty strong indicators.
Their findings suggested that people who carried these gene versions strongly tended to (a) get sicker early in the infection, (b) produce more cytokines early in the infection and (c) come down with ME/CFS. In short the genetic predisposition of these patients seemed to set them up for a particularly strong pro-inflammatory immune response early in an infection.
The Next Step. But then what? What might high cytokine levels do? I asked Dr. Lloyd, Dr. Vollmer-Conna and Dr. White about this. The Dubbo’s team current theory is that high cytokine levels early in the infection alters patterns of brain functioning. Specifically they believe they thrust the brain into a state of hyper-vigilance in which it over-reacts to signals coming from the body. They suggested ME/CFS was a kind of post-traumatic stress disorder with the proviso that the brain was overreacting to internal, physiological signals (as opposed to cues in the outside environment.)
This theory, which is close to the interoceptive theory, suggests that the state of illness disappeared from the body but not from the brain. The brain – believing the body is still sick – continues to produce sickness signals; it is these unrelenting signals that damage the HPA axis, immune system, and the other systems involved in chronic fatigue syndrome (ME/CFS) etc. over time.
Dr. White noted that these signals all occur under the level of consciousness – in the subconciousness. Given the benefits I’ve accrued from the Gupta Amygdala Retraining program which attempts to combat negative subconscious activities I asked them what they thought about it. I noted that meditation and other techniques (which the Gupta program among others employs) have been shown to reset autonomic nervous system functioning (i.e. retrain the brain). Dr. White felt that the program was good but that the problem may not specifically originate in the amygdala.
Dig Deeper: The Amygdala Retraining Program – A blog plus patient reports
The location of this central nervous system deficit is a matter of dispute. Ashok Gupta believes it originates in the amygdala, Dr. White in the anterior insular, Dr. Baraniuk in the Papez Circuit, Dr. Lloyd in another region, Dr. Chaudhuri and apparently Dr. Reeves in the basal ganglia. Most of these are in similar parts of the brain that effect cognition, emotions and autonomic nervous system functioning. A good deal of brain imaging research is going on right now and we should know fairly soon if these researchers are on the right trail
Questions/Questions – Given the Dubbo studies inability to find overt immune dysfunction/pathogen activity in a post-infectious set of ME/CFS patients does this mean that the immune/infection question has been answered? Apparently not to everyone’s satisfaction.
The CDC is taking another look at the Dubbo team’s long term cytokine data and the HHV-6 Foundation questions whether the right cytokines were measured. The Foundation believes it’s possible that original infections reactivated a central nervous system pathogen (HHV-6, enterovirus, endogenous retrovirus). They also question whether they were cleared out. Specifically they question whether the tests used to assess EBV activity would adequate to detect an active infection. They suggest that EBV EA antibody tests should have been used.
(The pathogen diagnosis questions really bedevil this field. During the lunches several researchers noted now difficult it was to find evidence of X pathogen in blood even when biopsies (or autopsies) revealed it was readily present in an organ. Throw in the possibility of a central nervous system infection and at least some researchers raise serious questions arise about the efficacy of blood-based tests. A recent study showed that HHV-6 can persist in the spinal fluid long after it’s disappeared from the blood. Another study found no evidence of HHV-6 infection in the spinal fluid even though later autopsies suggested it had been active in the brain )
(Dr. Klimas asked if the team had looked to see if virus’s such as HHV-6 had reactivated as the patients got ill. Could the initial pathogen have cleared out a space for another virus to pop up? Dr. Lloyd didn’t know and felt the jury was still out on that question. )
Biomarker (!)(?)
Nancy Klimas, Immune Markers in Viral Reactivation
Dr. Klimas looks at ME/CFS from the eyes of an immunologist and what she sees is an immune system that’s been revved up too long and has begun to bug out. Simply put ME/CFS patients immune systems are like auto’s with 250,000 miles on them and are fraying at the seams.
What in the body is putting chronic fatigue syndrome (ME/CFS) patient’s immune systems through their paces? Dr. Klimas believes a chronic viral infection is the culprit but in something of a departure from others believes it is found not in just 15-20% of patients but in a ‘large subgroup’ of them.
The evidence for immune activation is long and includes increased levels of cell suicide, poor NK and T-cell functioning, increased pro-inflammatory cytokine production and macrophage abnormalities.
NK cell dysfunction is a key immune problem in ME/CFS but it has a catch – a big catch – it’s expensive to test for. This has lead Dr. Fletcher and Dr. Klimas to look for a cheaper test that reflected poor NK cell functioning and they think they’ve found one – neuropeptide Y. In doing so they got an added bonus: the cheaper test may provide a clue to what’s causing the problem.
“A Very Good Biomarker for ME/CFS”
We regularly hear that this or that might be a biomarker for ME/CFS but as the years drag on there’s still no biomarker. Now Dr. Klimas says CD26 – a receptor found on immune cells and in soluble form in the blood – is ‘a very good biomarker for this disease’. This receptor apparently reflects immune depletion and is significantly, very significantly decreased (p<.0001) in ME/CFS patients.
Establishing A Neuro-immune Connection – Neuropeptide Y – The biomarker is big but there was also big news regarding a substance called Neuropeptide Y (NPY). We hear a lot about a neuro-immune connection in ME/CFS but little direct evidence of it. Neuropeptide Y may provide the bridge between the two that researchers are looking for.
NPY is stored in the nerve terminals of the sympathetic nervous system (SNS) and is released in conjunction with SNS nerve agents called catecholamines (norepinephrine, epinephrine). Recent evidence suggests that the activity of the SNS – which is part of the stress response – is increased in ME/CFS. Given that it stands to reason that NPY levels would be increased in ME/CFS as well – and they are – quite significantly so (p<.001). Intriguingly given the stress connection NPY levels are associated with an increased stress index and, given that, not surprisingly with increased anger, confusion, frustration, etc.
Dig Deeper: Nancy Klimas on immune dysfunction and the future in chronic fatigue syndrome (ME/CFS)
The Fletcher/Klimas team is one of the few that’s been able to crack the NIH. They’ve been getting NIH grants to study ME/CFS patients for over 15 years now. I asked Dr Fletcher if getting a grant was any easier now. She looked at me and laughed and said ‘Are you kidding?’. Their latest grant – which examines immune measures when ME/CFS patients are experiencing ‘good days’ and ‘bad days’ – took three rounds to get approved. She said it was roundly rejected until it was finally approved and that the makeup of the committee was key.(Advocates have saying this for years. Not only is it rare for panelists that sit on the Chronic fatigue syndrome Special Emphasis Panel to have expertise in ME/CFS its equally rare for them to know anything about the immune system. (Thats right – few panelists that sit on the CFS review committee typically know anything about CFS))
Dirt in the Gears 
Suzanne Vernon – Genetic variation and altered immune activity in Chronic Fatigue Syndrome
Dr. Vernon’s talk really got some people buzzing. She’s been searching for patterns in large, complex data sets that contain gene expression, gene polymorphism and laboratory data. This is the kind of unique cutting edge stuff that exemplified the Pharmacogenomics efforts. This is not cutting edge ME/CFS stuff its cutting edge period. It’s a new way of looking at complex multi-systemic diseases.
Her evidence suggests ME/CFS really is a multi-systemic disease but on a scale that hasn’t been comtemplated before. We’re going to wait for the papers publication- hopefully in a few weeks – but suffice it to say that her recent evidence suggests that entire systems – not just x or y types of cells – but entire systems are operating abnormally in ME/CFS. It’s a fascinating thesis.
The HPA axis – a important part of stress response system – appears to be ground zero in this scenario of systemic derangement. Dr. Vernon was the leader the CDC’s Pharmacogenomic’s projects which ended up again and again pointing at the HPA axis, in particular, at the adrenal stress hormone cortisol. Since then the CDC has run off a nice string of ‘successful’ papers on the subject. In the abstract for her talk Dr. Vernon put the HPA axis front and center stating that “hypoactivity (reduced activity) of the HPA axis leads to neuroendocrine and immune alterations”.
What’s the evidence for that? And what kinds of alterations is she talking about? We’ll have to wait for the paper.
Dig Deeper: the Pharmacogenomics Papers – the Overviews
The Fatigue Syndromes
An Overview of Post-Viral Fatigue: CFS or What? By Peter White 
As time goes on researchers are trying to dig deeper and deeper into the ‘fatigue syndromes’. Dr. White a well known UK psychiatrist asked whether the post-viral fatigue commonly after infectious mononucleosis (glandular fever) is different from chronic fatigue syndrome (ME/CFS).
The fatigue after infectious mononucleosis is not trivial; studies show that about 40% of IM patients will complain of fatigue six months after the onset and that 12% will go so far as to see the doctor for it within a year. Most do appear to recover over time.
Mood disorder, PVFS and ME/CFS – Most people who get post infectious fatigue syndrome (PIFS) do not come down with CFS. They often suffer from depression early on but it disappears quickly. Interestingly Dr. White stated the depression process found in ME/CFS is kind of unique; they could find all sorts of factors that could predict who will get depressed in PIFS but they couldn’t find them in ME/CFS. Indeed Dr. White was clear that ME/CFS is not – as was proposed for years – a kind of atypical depression.
Dr. Enlander asked about the relationship between mood disorder and ME/CFS. Dr. White felt it was quite complicated. Depression is a risk factor for chronic fatigue syndrome but it is not a ‘big driver’ for it; i.e. other still unelucidated factors than depression are much more important in producing the disease. He noted that many ME/CFS patients are not depressed.
PVFS and ME/CFS: similar but different – That both PVFS and ME/CFS patients were more likely to have seen their doctor for fatigue before they became ill suggested that some processes that later became amplified were already present. A finding that PVFS patients tended to experience more infections than normal before they come down with PVFS suggested they may have had immune problems beforehand. (Dr. Chia will report he sees the same process). CFS patients, on the other hand, tended to have more mood disorders than PVFS patients or healthy controls before they became ill. PIFS patients also tended to suffer from insomnia while CFS patients tend to experience hypersomnia (increased sleep).
Interestingly data is emerging to suggest that not all infections trigger chronic fatigue syndrome. Flu pathogens, for instance, do not appear to. ‘Just for fun’ Dr. White guessed that about 20,000 people in the US come down with chronic fatigue syndrome (ME/CFS) after having infectious mononucleosis every year (60/day).
Activity and ME/CFS – Dr. Bell asked what role activity level prior to getting sick played in the disease. Dr. White replied that evidence is emerging that both decreased and increased activity levels put one at increased risk of ME/CFS. He noted that people who experienced fatigue and kept exercising had an increased risk of coming down with ME/CFS.
Dr. Lloyd noted that behavioral therapies were very helpful early in the illness. This was an interesting statement given evidence that people who try to bull their way through it (or exercise) place themselves at increased risk. Apparently the behavioral paradigm for ME/CFS no longer includes ignoring or denying the manifestations of the illness (???).
One wonders if these behavioral therapies are actually reducing activity levels? Or if their new focus on ensuring one gets enough sleep, for instance, is particularly early in the disease? In an upcoming interview Dr. Friedman will point out that most ME/CFS patients are too active for their own good.
Thanks to the HHV-6 Foundation and PANDORA for their assistance in attending the Baltimore Conference, thanks to Tom Hennessey for getting me back and forth several times from DC and thanks to my brother for his twisted but still much appreciated hospitality. Thanks to the HHV-6 Foundation for their comments on this paper.
To The Symposium on Viruses in Chronic Fatigue Syndrome (ME/CFS): Part I
Dr John Chia at the International Symposium on Viruses In CFS