M.E. caused by enterovirus?

Hip

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No. They are considered to be triggers of ME.
According to leading researchers like Dr John Chia and Dr Jonathan Kerr, these two infectious agents are considered known causes of ME/CFS:

Chronic Chlamydia pneumoniae infection: a treatable cause of chronic fatigue syndrome.
Chia JK, Chia LY

Chronic fatigue syndrome and arthralgia following parvovirus B19 infection
Kerr JR, Bracewell J, Laing I, Mattey DL, Bernstein RM, Bruce IN, Tyrrell DA.

Successful Intravenous Immunoglobulin Therapy in 3 Cases of Parvovirus B19–Associated Chronic Fatigue Syndrome
J. R. Kerr, V. S. Cunniffe, P. Kelleher, R. M. Bernstein, and I. N. Bruce

More proof that parvovirus B19 and Chlamydia pneumoniae cause ME/CFS also comes from the fact that these pathogens are treatable, and once you treat these infections, the ME/CFS symptoms disappear.


Why do some who have the infection, not develop the disease state that is known as ME?
Why do most individuals (90%) who catch poliovirus show no symptoms at all (asymptomatic), but a very small percentage (1%) will get paralytic poliomyelitis from the poliovirus?

Answer: because there are obviously other factors involved, and these other factors determine whether poliovirus causes paralytic poliomyelitis or not.

However, in spite of the fact only a small percentage develop paralytic poliomyelitis from poliovirus, nobody would argue that poliovirus is not the cause of paralytic poliomyelitis.

Likewise, if enterovirus does turn out to be a major cause of ME/CFS, that does not imply that enterovirus will always cause ME/CFS in everyone who catches it. Even HIV does not cause AIDS in everyone, because certain individuals are largely immune to HIV.
 
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Firestormm

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As you said "if enterovirus does turn out to be a major cause of ME/CFS"...

I would be more than happy to personally contribute to a decent research project if someone like Lipkin (for example) were to say it was a theory worth pursuing.

Would you like to draft something I can forward to Ian Lipkin to see what his opinion on the previous research and the theory from Chia might be? It might see him meet with Chia and move things forward.

Though I still can't understand why Chia has not done more to pursue this line of research himself. Perhaps it is asking to much but he did say I think that little interest has been shown in this research - even from those involved in ME - there must be a reason for this: I mean people have been in pursuit of 'the cause' for 50 years so why hasn't this been jumped on?

I was disappointed to see Kerr leave the field and that nobody picked up his research and ran with it - as I am sure you would be if the same happened to Chia's work.
 
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That would be a sad day indeed. I do not understand(I may have missed the point in this thread)why nobody else seems to be interested in Dr Chia's work... If some one shares a personal stake in an illness does that some how imply a bias?? I mean even KDM refered to Dr Chia's work as 'that American' with out even making reference to his name :(
 
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Not too many people were that interested in MLK, Ghandi and Mandela but they got there in the end. :)

The research and interest with regards to ME/CFS is rather fragmented and this is really the issue. I believe this is because ME/CFS and other immune system related illnesses have not been that well known about in the past and in fact are now on the increase; which I believe is due to the immune system having to deal with a whole new variety of chemicals and toxins and virus mutations which it had not evolved to deal with.

As we all know there have been many high profile people who have dx'd from cancer, etc., whereas I do not see so many having issues with ME/CFS. If for example the Queen of England, President of the USA or George Clooney was suddenly struck down with ME/CFS then we many see a quicker increase in interest. This is why all the ME/CFS organisations need to get together to form one coordinated body/voice.

Regards.
 

Hip

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Enterovirus is the most studied virus in ME/CFS, and has consistently been linked to ME/CFS:
List of ME/CFS Enterovirus Research Papers
Dating from 1955 to present


Note that ▶︎ indicates a positive study (eg, one finding enterovirus much more commonly in ME/CFS patients than in healthy controls), and ▶︎ indicates a negative study (no difference between patients and controls).
Royal Free Hospital London — Epidemic Outbreak of ME/CFS in 1955:

Epidemiological aspects of an outbreak of encephalomyelitis at the Royal Free Hospital, London, in the summer of 1955
Nuala Crowley, Merran Nelson, and Sybille Stovin. J Hyg (Lond). 1957 March.

An Outbreak of Encephalomyelitis in the Royal Free Hospital Group, London, in 1955
The Medical Staff Of The Royal Free Hospital. Br Med J. 1957 October.

In the Royal Free outbreak, coxsackievirus B was suspected, but at that time no serological evidence was obtained.
Early ME/CFS Enterovirus Research (Which is Mainly British):
Dating from 1970 to 2003

Encephalomyelitis Resembling Benign Myalgic Encephalomyelitis
S.G.B. Innes. The Lancet. 1970 May.
▶︎ This study examined 4 cases of ME. In the cerebrospinal fluid they found coxsackievirus B2 in one case and echovirus 3 in another. In the sera of the two other cases they found elevated coxsackievirus B2 and elevated coxsackievirus B5 titers via antibody testing.

Sporadic myalgic encephalomyelitis in a rural practice
B. D. Keighley and E. J. Bell. J R Coll Gen Pract. 1983 June.
▶︎ This study found elevated coxsackievirus B titers in 16 of of 20 patients in an ME/CFS outbreak in Ayrshire, UK.

Myalgic encephalomyelitis—report of an epidemic
K. G. Fegan, P. O. Behan, and E. J. Bell. J R Coll Gen Pract. 1983 June.
▶︎ This study found elevated coxsackievirus B titers in 18 out of 20 patients in an ME/CFS outbreak in Ayrshire, UK.

Coxsackie B infection in a Scottish general practice
B. D. Calder and P. J. Warnock. J R Coll Gen Pract. January 1984.
▶︎ This study found high antibody titers to coxsackievirus B in 38 out of 81 patients who experienced a syndrome with many of the features of myalgic encephalomyelitis.

Some long-term sequelae of Coxsackie B virus infection
J. A. Gray. J R Coll Gen Pract. 1984 January.
Discussion of coxsackievirus B and echovirus in relation to ME/CFS.

A study of Coxsackie B virus infections, 1972-1983
Bell EJ and McCartney RA. J Hyg (Lond). 1984 October.
▶︎ Found that in well-documented cases of ME/CFS, 41% of patients had elevated neutralizing antibody titers, compared to 4% of healthy controls.

Coxsackie B viruses and myalgic encephalomyelitis
E J Bell, R A McCartney, and M H Riding. J R Soc Med. 1988 June.
▶︎ This study on 290 adults and 47 children with ME/CFS found 37% and 38% respectively were IgM positive for coxsackievirus B, compared to 9% in 500 healthy adult controls.

Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA (full text here).
Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC. J Gen Virol. 1990 June.
This study found that normally, positive strand enterovirus RNA is 100-fold more common over negative strand enterovirus RNA; but in ME/CFS patients, equal amount of both were found. This study I believe was the first to demonstrate an unusual viral phenomenon in ME/CFS that would later be termed and understood as a non-cytolytic enterovirus infection (aka: non-cytopathic, or defective enterovirus infection).

Myalgic encephalomyelitis--a persistent enteroviral infection?
Dowsett EG, Ramsay AM, McCartney RA, Bell EJ. Postgrad Med J. 1990 July.
▶︎ This study found that out of 420 cases of ME/CFS, 205 had significant titers to coxsackievirus B.

Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome
Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO. BMJ. 1991 March.
▶︎ This study on 60 ME/CFS patients found 20% had high titers to coxsackievirus B, compared to 14% of healthy controls. Furthermore, 53% of these ME/CFS patients had enteroviral RNA sequences in their muscles, compared to 15% for healthy controls.

Amplification and identification of enteroviral sequences in the postviral fatigue syndrome
Gow JW1, Behan WM. Br Med Bull. 1991 October.
▶︎ This study of 60 ME/CFS patients found that ME/CFS patients were 6.7 times more likely to have enteroviral RNA in their muscle tissue, compared to healthy controls.

Persistent virus infection of muscle in postviral fatigue syndrome
Cunningham L, Bowles NE, Archard LC. Br Med Bull. 1991 October.
▶︎ This study of 140 ME/CFS patients found enteroviral RNA in 24% of their muscle biopsy samples, and Epstein-Barr virus DNA in a further 9% of these biopsy samples, whereas enterovirus RNA was not detected in any of 152 control samples of human muscle.

Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy
Bowles NE, Bayston TA, Zhang HY, Doyle D, Lane RJ, Cunningham L, Archard LC. J Med. 1993.
▶︎ This study of 158 ME/CFS patients found enteroviral RNA in 26% of the patients' muscle biopsy samples, compared to only 1% in healthy controls.

Studies on enterovirus in patients with chronic fatigue syndrome
Gow JW, Behan WM, Simpson K, McGarry F, Keir S, Behan PO. Clin Infect Dis. 1994 January.
▶︎ This study of 121 patients with ME/CFS found enteroviral RNA in 26.4% of the patients' muscle biopsy samples, and found enteroviral RNA in 19.8% the muscle biopsies of patients other neuromuscular disorders. From these results the authors concluded that "it is unlikely that persistent enterovirus infection plays a pathogenetic role in CFS, although an effect in initiating the disease process cannot be excluded."

However, this conclusion may not be a sound, firstly because persistent enterovirus is associated with a wide range of diseases, including chronic inflammatory myopathy, and thus might be playing a role in these other neuromuscular disorders as well; and secondly because persistent enterovirus infections are also found in other organs in ME/CFS patients, such as the brain and stomach (though this fact was not known at the time of publication), and it is possible ME/CFS might in fact be caused by an enterovirus brain infection, rather than (or in addition to) a muscle infection.

Enterovirus in the chronic fatigue syndrome (full text here and here)
McGarry F, Gow J, Behan PO. Ann Intern Med. 1994 June.
▶︎ This study details an autopsy of a deceased ME/CFS patient. Enteroviral RNA was found in the heart, muscles, hypothalamus and brainstem of this patient, and this RNA showed an 83% similarity to coxsackievirus B3. Control tissue samples taken from four patients who died of cerebrovascular diseases, and another four who had depression and committed suicide, showed no evidence of enteroviral RNA.

Enteroviruses and the chronic fatigue syndrome
Swanink CM, Melchers WJ, van der Meer JW, Vercoulen JH, Bleijenberg G, Fennis JF, Galama JM. Clin Infect Dis. 1994 November.
▶︎ This study, conducted by some of the psychologists at the Nijmegen Group (who consider ME/CFS to be psychogenic), did not find any difference between the blood and stool samples of 76 ME/CFS patients and 76 healthy controls; but the enterovirus detection methods they used are now known to be quite insensitive in terms of detecting chronic enterovirus infections.

Detection of enterovirus-specific RNA in serum: the relationship to chronic fatigue
Clements GB, McGarry F, Nairn C, Galbraith DN. J Med Virol. 1995 February.
▶︎ This study of 88 ME/CFS patients found enteroviral RNA in the serum of 41% of patients, compared to 2% of healthy controls.

Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome
Galbraith DN, Nairn C, Clements GB. J Gen Virol. 1995 July.
This study found that ME/CFS patients with persistent enteroviral infections nearly always have viruses with a different genetic makeup compared to enteroviruses found in acute, self-limiting infections in healthy controls.

Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome
McArdle A, McArdle F, Jackson MJ, Page SF, Fahal I, Edwards RH. Clin Sci (Lond). 1996 April.
▶︎ This study examined 34 muscle biopsies from ME/CFS patients and 10 muscle biopsies from healthy controls, but did not detect enterovirus RNA in the patient or control muscle tissues. But commenting on the differences between their negative and the positive results found in Gow 1991, the authors say:
"The difference in findings between our study and that of Gow et al. [21] may be due to the population of CFS patients studied. Although the diagnostic criteria of both groups was broadly similar, the patients used in the study of Gow et al. [21] all reported that the illness had an acute onset after a feverish illness, whereas only 58% of patients in our study reported a viral infection before the onset of their illness."

No findings of enteroviruses in Swedish patients with chronic fatigue syndrome
Lindh G, Samuelson A, Hedlund KO, Evengård B, Lindquist L, Ehrnst A. Scand J Infect Dis. 1996.
▶︎ This Swedish study examined 29 muscle biopsies from ME/CFS patients, but could not detect enterovirus RNA in the tissues.

Viral Isolation from Brain in Myalgic Encephalomyelitis (A Case Report)
Richardson, J. Journal of Chronic Fatigue Syndrome, Vol. 9(3/4) 2001.
▶︎ This study examined the brain of an ME patient who died through suicide, and found enteroviral VP1 protein in the fibroblasts of small blood vessels in the cerebral cortex, plus some patchy distribution of enteroviral VP1 protein in a small fraction of glial cells.

Enterovirus related metabolic myopathy: a postviral fatigue syndrome
Lane RJ, Soteriou BA, Zhang H, Archard LC. J Neurol Neurosurg Psychiatry. 2003 October.
▶︎ This study of 48 patients with ME/CFS found enteroviral sequences by RT-NPCR in 20.8% of patients' muscle biopsy samples, while all the 29 control samples were negative for such sequences.
Dr John Chia's ME/CFS Enterovirus Research
From 2005 onwards


The role of enterovirus in chronic fatigue syndrome.
Chia JK. J Clin Pathol. 2005 November.
▷ A review paper summarizing experimental and clinical evidence supporting the role of enterovirus in chronic fatigue syndrome.

Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach.
Chia JK, Chia AY. J Clin Pathol. 2008 January. Full paper here.
▶︎ This study of 165 ME/CFS patients found enterovirus VP1 protein in 82% of stomach tissue samples from patients, compared to 20% in healthy controls. 37% of the ME/CFS patient stomach tissue samples tested positive for enterovirus RNA, compared to less than 1% for healthy controls.

Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence.
Chia J, Chia A, Voeller M, Lee T, Chang R. J Clin Pathol. 2010 February.
▶︎ This study followed patients who were hospitalized for acute enterovirus infections, and found that in the next few years subsequent to the acute infections, symptoms consistent with ME/CFS emerged in 3 patients.

Chronic enterovirus infection in a patient with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) – clinical, virologic and pathological analysis
John Chia, David Wang, Andrew Chia, Rabiha El-Habbal. 2015.
▶︎ This brain autopsy on a deceased ME/CFS patient found evidence of enterovirus infection in various areas of the brain.
CHRONIC ENTEROVIRUS INFECTION IN A PATIENT WITH MYALGIC ENCEPHALOMYELITIS/ CHRONIC FATIGUE SYNDROME (ME/CFS) – CLINICAL, VIROLOGIC AND PATHOLOGICAL ANALYSIS

John Chia, David Wang, Andrew Chia, Rabiha El-Habbal

OBJECTIVES: A 23 y/o Caucasian male developed prolonged, recurrent gastrointestinal symptoms, followed by onset of severe ME/CFS (CDC criteria, ICC). At initial evaluation, Echovirus 11 antibody titer was ≥1:640 (normal <1:10); IgG and IgM antibody for EBV and HHV6 were negative, CMV IgG was positive. He failed to respond to a combination of α and γ interferon; and debilitating symptoms of the stomach and central nervous system were minimally alleviated by SSRI, benzodiazepine and acid-suppressants. Repeated MRI scans of brain and spinal cords showed normal results. The patient committed suicide 6 years after the onset of symptoms. Brain was harvested and frozen within 24 hours of death for evaluation of chronic viral infection.

METHOD: Using 5D8/1 and J2 monoclonal antibody, stomach and colon biopsies obtained 5 months after onset of illness were stained for viral capsid protein (VP1) and dsRNA, respectively, by immunoperoxidase technique. Blood drawn in Paxgene tube 3 years after illness was screened for enterovirus RNA by RT-PCR. 1 cm3 sample was taken from the ponto-medullary junction (PM), medial temporal lobe (MT), frontal lobe (FL), occipital lobe (OL), cerebellum (CL) and midbrain/hypothalamus area (MB) of brain. The brain samples were homogenized in 10 ml of serum-free medium. Aliquots were processed for viral cultures. Trizol-LS reagent was used for RNA and protein extraction, as well as other lysis agents. Protein samples were separated with Tris-Glycine and MES gels, wet and semi-dry transfer, then western blot was performed with Ibind (Life technology) using EV-, CMV- and HHV6-speci c mAbs, patient’s own serum and control serum samples. Viral culture was performed in WI-38 and BGMK-DAF cell lines. RT-PCR for conserved highly-conserved sequences of 5’ end and 3D polymerase sequence were performed on extracted RNA.

RESULTS: Stomach and colon biopsies stained positive for EV VP1 soon after initial infection documenting the initial viral infection; dsRNA was detected in the stomach biopsies. EV RNA was not detected in blood 3 years after illness. Initial culture of brain samples did not grow virus; 5’ EV RNA sequence was not detected by RT-PCR. Using 5 D8/1 mAb, western blot revealed 37K protein band in the brain samples, which corresponded to viral protein extracted from infected stomach biopsies and enterovirus culture, but not in brain biopsy samples taking from patients with brain tuberculoma and lymphoma. 3D pol gene was ampli ed from the DNase-treated RNA extracted from PM, MT and FL.

CONCLUSION: The analysis of the second brain specimen taken from a ME/CFS patient replicated the British findings published in 1994 (Ann. IM). The finding of viral protein and RNA in the brain specimens 6 years after documented acute enterovirus infection of the gastrointestinal tract is consistent with a chronic, persistent infection of the brain causing debilitating symptoms. EV is clearly one of the causes of ME/CFS, and antiviral therapy should be developed for chronic EV infection.

Source: 19th International Picornavirus Meeting, 2016


For more details on the three separate brain autopsy studies on deceased ME/CFS patients, which found enterovirus / coxsackievirus B infection in the brain, see here.

A similar MEpedia list of studies linking enterovirus to ME/CFS.

An MEpedia article on ME/CFS postmortem brain autopsies.
 
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Firestormm

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Thanks @Hip It is always handy to have it all in once place. It doesn't explain why this has not progressed unfortunately - and the offer still stands if you want to draft something for Dr. Lipkin to review - assuming he is able of course - I will pass it along (or you can yourself of course - not saying I have his ear or anything).
 

Ema

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Yes, what you said @end is right:

The enterovirus antibody tests (micro-neutralization tests) at ARUP Lab (for coxsackievirus B and echovirus) do determine which species of enterovirus you have.

However, this antibody tests are not as sensitive as the enterovirus VP1 protein stain test (aka immunohistochemistry test), which tests a biopsy tissue sample from your stomach for the presence of enteroviruses.

More info about this here:
Enterovirus Foundation
So for someone not able to have the gut biopsy test, is it worth doing the ARUP panel *first* as a means to try to convince a doctor to do the more sensitive biopsy?
 

Wally

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Thanks @Hip It is always handy to have it all in once place. It doesn't explain why this has not progressed unfortunately - and the offer still stands if you want to draft something for Dr. Lipkin to review - assuming he is able of course - I will pass it along (or you can yourself of course - not saying I have his ear or anything).
http://www.mailman.columbia.edu/our-faculty/profile?uni=wil2001

Dr. Ian Lipkin


Contact Information

Office/Address:

Center for Infection and Immunity, 722 West 168th Street, Room 1703a

New York, NY 10032

USA

Website Address:

Homepage URL

Phone:

212-342-9033

Fax:

212-342-9044

E-mail:

wil2001@columbia.edu
 

Hip

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So for someone not able to have the gut biopsy test, is it worth doing the ARUP panel *first* as a means to try to convince a doctor to do the more sensitive biopsy?
I understand that Dr Chia uses just the ARUP Labs enterovirus tests for many patients, because the stomach biopsy is more difficult to do (you have to first find a willing gastroenterologist, and then you have to go through a procedure involving sticking an endoscope down your throat in order to take a stomach tissue biopsy).
 
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So for someone not able to have the gut biopsy test, is it worth doing the ARUP panel *first* as a means to try to convince a doctor to do the more sensitive biopsy?
Hip, it may also be worth mentioning that most LABS HOLD BIOPSIES for DECADES in some cases

They are very stable. Mine were sent to Dr Chia from a Lab here in Australia that had my samples 'on ice' from an endoscopy in the past
 

Izola

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The claims it was refuted do not seem to be backed up by appropriate references. I think the wikipedia is wrong. One of those references was in fact from a paper by Wessely, and it was less a refutation than a restamping with his own brand.

I am aware that Ramsay, Hyde and Hooper all dispute the McEvedy and Beard claim. However it does not seem to have had much impact.

How many doctors actually read such papers? In particular, how many psychiatrists read biomedical papers? I don't think the disputation is widely known. The only one with substance was published in the South African Medical Journal. How many mainstream docs actually read that?

I think the McEvedy and Beard paper set things up for the railroading in the 80s. I think it had influence both in the UK and the US, but I still need to do a lot more research about this. It changed attitudes, and those attitudes made many vulnerable to the claims in the 80s.

Aside from enteroviral research, I think that from 1963 the technology was available, and in wide use, to properly assess ME patients. A combination of different issues of ignorance led this to being largely ignored till about 2007. I am referring to the 2 day CPET. CPET started in the 40s but became a standard protocol about 1963, in the Bruce protocol (though the modern protocol is better). Taking into account Ramsay's observations, and the (new in 1963) protocol to assess cardiopulmonary function, ME should have been validated before even 1970.

One of the issues, as we know well in ME research, is that published scientific papers seem to have little impact on a medical community that largely is too busy, too disinterested, and too sure they know what they are doing. Doctors often don't read science, they are often only interested on material with immediate clinical use, and they don't have time to research in obscure journals. Only dedicated doctors with a personal interest, or researchers, seem to take the time.
If doctors were lawyers they would be disbarred.
 

Izola

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No. They are considered to be triggers of ME. There is a difference. Until such time as they can be identified as causing the disease itself, they remain triggers along with other known triggers.

There is something else occurring, other than the infections themselves. Not everyone who has glandular fever goes on to develop the symptoms and prognosis associated with ME. There elusive connections are between the infection and the disease state.

Why do some who have the infection, not develop the disease state that is known as ME? ME occurs after a period of time has elapsed during which a recovery would be deemed likely. It is part of the reason - I believe - why you cannot diagnosis ME from day one: but diagnosis only occurs after several months (ideally) following the trigger and this lack of recovery.

We are now at a different place in our understanding from that of the ME outbreaks where it was thought that some common but unknown 'agent' might have been responsible. In history there have been many incidences of people not recovering well - as others might - from an infection and it didn't matter what the infection might have been.

If Chia can demonstrate that enteroviruses are somehow being reactivated by something in only certain people and leading to the disease state known as ME: then that might prove part of the puzzle for some.

Why he hasn't tried to apply to NIH or elsewhere for a grant to carry out a proper controlled trial I do not know: but maybe if patients were willing they could persuade him to make an application.

He still needs to demonstrate a pathological link and to try and show what is causing this reactivation of a virus that can only be found in the gut through biopsy, and only then is reactivated in some patients.

Why don't one of you simple fire a question off to Lipkin or Mady Hornig, and ask if it is even possible for a virus to hide in the stomach, and be reactivated, and if so by what, and then if it could go on to present as ME symptoms?

You guys know this stuff better than me, but has it even been demonstrated that 'something' can reactivate enteroviruses or that they can hide in tissue?

Maybe if you asked the relevant question of Lipkin and his team, he might then approach or invite Chia for a chat and a review of his research?

If you want, draft something, and I will forward it to Columbia. We are developing quite a good rapport with the Microbiome study campaign. Just keep it brief and to the point.
Yeah!
 

Raindrop

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Judy,
Finally getting back to this. It would be very hard to get to Dr. Chia. I last understood that there was
nothing via *blood tests* that he could "work with" very well. Thought that he HAD to order endoscopy
(?) to be able to diagnose and to treat. Are you saying that he DOES have a way of figuring out
if you have the Coxsackie enterovirus through blood work alone? (I once a year or two called his
office and thought they said the endoscopy was necessary) Are there OTHER
viruses he is looking for other than the standard CFS work up type we have probably
all had ? (Maybe it would be helpful to just know which ones he tests for) If he can figure out if you have it,
my understanding was that there is no way to TREAT it, other than with his Herbs out of China
I think and these have not been very successful from what I heard. Very much appreciate the
information. Maybe reconsider Chia and the effort to go there.
 

Izola

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HI: Not the same thought that I forgot, I think!!. . . McEvedy and Beard paper " "theory made their dishonest and stupid thoughts into my 1rst year Soc text in 1973 as established fact. My young mind read that and said "No way, no how. You can't catch unspoken thoughts through the air and make a somatic disease from it--the miasma theory of disease has long been disproven." I want my tuition back for that semester!!