by Margaret Williams
For decades it has been known and shown that viruses play a role in ME/CFS; some illustrations from the literature are provided below (all of which are relevant and significant).
In relation to “CFS”, the most-studied viruses have been the Epstein-Barr Virus (EBV) and the Human Herpes Virus-6 (HHV-6). In relation to “pure” ME, the most studied viruses (and for which there is extensive evidence) have been the enteroviruses, usually Coxsackie B (CBV). Some illustrations from the literature of the role that viruses play in ME/CFS are provided at the end of this paper; all are significant.
There is increasing awareness that the dysregulated immune system that is a hall-mark of ME/CFS allows multiple latent viruses and microbial agents to become reactivated (Co-Cure NOT:12th November 2009).
Moreover, recent research has shown that even viruses which were hitherto believed not to persist after an acute infectious episode are capable of long-term viral persistence.
Nora Chapman et al from the Enterovirus Research Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Centre, have shown that human enteroviruses Coxsackie B can naturally delete sequence from the 5’ end of the RNA genome and that this deletional mechanism results in long-term viral persistence, which has substantially altered the previously held view (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2440640/?tool=pubmed).
In a specially commissioned piece for the charity Invest in ME, the researchers say:
“This previously unknown and unsuspected aspect of enterovirus replication provides an explanation for reports of enteroviral RNA detected in diseased tissue in the apparent absence of virus particles”
(Journal of IiME 2009:3:1).
“I believe that the main reason (ME)CFS patients are symptomatic is due to continuing inflammatory response toward viruses living within the cells, enteroviruses in most of the cases I see. We have clearly documented certain enterovirus infections triggering autoimmune responses in some patients…Can you imagine how we would feel if there are viruses surviving in our muscles, brains, hearts and gastrointestinal tracts triggering ongoing immune responses?”
(http://aboutmecfs.org/blog/?p=865).
“A virus is a microscopic organism that lives within the cells of another living organism. Viruses cause disease at the most basic level, by damaging the cells of living things. By themselves, viruses are lifeless particles incapable of reproduction, but once they enter the cell of another living thing they become active organisms that can multiply hundreds of times.
“Viruses are comprised of two parts – a core of either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) and a protective envelope of protein. RNA viruses are smaller than DNA viruses and sometimes contain a special enzyme called reverse transcriptase which allows them to convert RNA to DNA. These specialised viruses are known as retroviruses and have a unique ability to merge with the host’s own genetic material.
“Retroviruses have the unique ability to replicate themselves by (i) making a double-stranded DNA copy called a ‘pro-virus’ once they enter living cells. Pro-viruses integrate themselves into the human chromosome and become part of the host’s genetic code (ii) alter the host’s immune response by evading detection as a ‘hidden invader’ (iii) remain hidden and latent, spliced within the host’s DNA, for long periods of time. Retroviruses are known to be potent stimulators of cytokines”.
On 8th October 2009 the premier journal Science published a paper online showing a direct link between a retrovirus and ME/CFS (Detection of infectious retrovirus XMRV, in blood cells of patients with chronic fatigue syndrome. Lombardi VC, Ruscetti FW, Peterson DL, Silverman RH, Mikovits JA et al) which caused global reverberations.
However, this was not the first time that a retrovirus had been associated with ME/CFS.
In 1991, using polymerase chain reaction and in situ hybridisation, Dr Elaine De Freitas, a virologist at the Wistar Institute, Philadelphia (which is America’s oldest independent institution devoted to biological research) and Drs Daniel Peterson, Paul Cheney, David Bell et al found such an association (Retroviral sequences related to human T-lymphotropic virus type II in patients with chronic fatigue immune dysfunction syndrome. Proc Natl Acad Sci USA 1991:88:2922-2926). It is notable that co-author Hilary Koprowski is a distinguished virologist and Professor Laureate who was Director of the Wistar Institute from 1957-1991; he is a member of the US National Academy of Sciences and is Director of the Centre for Neurovirology at Thomas Jefferson University.
Before publication, the findings were presented on 4th September 1990 by Elaine De Freitas at the 11th International Congress of Neuropathology in Kyoto, Japan.
Ten days later, on 14th September 1990 Dr Peter White (as he then was) and other members of the Wessely School dismissed the findings:
“in the vast majority of CFS cases there is a psychological component. About 75% of CFS sufferers are clinically depressed, according to Peter White, senior lecturer in the department of psychiatric medicine at St Bartholomew’s Hospital in London. White said he believes depression is often a cause, rather than a consequence, of CFS…
Les Borysiewicz, a clinical virologist at Addenbrookes Hospital in Cambridge (now Chief Executive of the MRC, having succeeded Professor Colin Blakemore) (said) ‘Whatever causes CFS, it isn’t the virus itself’…
Anthony Clare, psychiatrist and medical director of St Patrick’s Hospital in Dublin (now deceased), pointed out that…there have been many ‘fatigue’ diseases with shifting causes: ’Neurasthenia, food allergies, now viruses. Some people would always rather have a disease that might kill them than a syndrome they have to live with’ ”
(Science 1990:249:4974:1240).
In their PNAS article that was published in April 1991, De Freitas et al noted that chronic fatigue immune dysfunction syndrome (CFIDS) “may be related or identical to myalgic encephalomyelitis” and examined adult and paediatric CFIDS patients for evidence of human retroviruses (HTLV types I and II).
As the CFIDS Chronicle article noted, the Wistar team looked at the peripheral blood DNA to see if they could find messenger RNA (mRNA) encoding for a viral segment of the HTLV-II virus.
At that time, known human retroviruses were the human immunodeficiency viruses 1 and 2 (HIV-1 and HIV-2) which are known to cause AIDS, and human T-lymphotropic viruses HTLV-I which causes lymphoma and HTLV-II which causes leukaemia (Hunter-Hopkins ME-Letter, October 2009). The four segments of the HTLV-II virus are referred to as the env, gag, pol and tax.
After a two year study, De Freitas et al provided evidence for HTLV-II-like infection of blood cells from CFIDS patients (and also to a lesser extent from people closely associated with them). This evidence was further substantiated by patient reactivity to proteins with the molecular weights reported for HTLV-I and HTLV-II antigens.
In their article, De Freitas et al said:
“The frequency of these antibodies in CFIDS patients compared with healthy non-contact controls suggests exposure / infection with an HTLV-like agent rare in healthy non-contact people”.
Whilst none of the CFIDS patients’ blood sample contained detectable HTLV-I gag sequences, DNA from at least two separate bleedings was positive for the HTLV-II gag subregion in 83% of adult and 72% of paediatric CFIDS patients, and the authors pointed out that “similar frequencies of PBMCs (peripheral blood mononuclear cells) expressing retroviral mRNA have been reported for HIV-infected individuals…The clinical histories of these CFIDS patients do not reveal behavioural or genetic factors usually associated with retroviral infection. Yet our data suggest that not only are these HTLV-II-like genes and HTLV-reactive antibodies associated with CFIDS in patients but that samples from a significant proportion of their non-sexual contacts are positive”.
De Freitas et al were careful to emphasise that
Also on 16th January 1992, the same Dr William Reeves of the CDC wrote to Joan Irvine about the same issue:
“…since on-going research indicates an infectious agent may be involved in some cases of CFS it would seem prudent to refrain from donating blood until this issue is resolved”
(http://www.cfs-news.org/joan.htm ).
It is worth noting that people in the UK with ME have been permanently excluded from donating blood since at least 1989 (Guidelines for the Blood Transfusion Service in the UK, 1989: 5.4; 5.42; 5.43; 5.44; 5.410).
This was subsequently upheld by the Parliamentary Under Secretary of State The Lord Warner, who confirmed in writing on 11th February 2004 in a letter to the Countess of Mar that people with ME/CFS
are not permitted to be blood donors. Lord Warner was unambiguous:
Given the (re)-discovery of a direct link between a retrovirus and ME/CFS, the importance of this cannot be over-stated.
Notably, those with a behavioural disorder are not prevented from donating blood.
XMRV (retrovirus associated with ME/CFS)
As mentioned above, in October 2009 the journal Science published a paper by collaborators from the Whittemore Peterson Institute, the US National Cancer Institute and The Cleveland Clinic that demonstrated a direct link between the retrovirus XMRV and ME/CFS (Science: 8th October 2009:10.1126/science.1179052).
XMRV stands for xenotropic murine leukaemia virus-related virus (xenotropic meaning a virus that can grow in the cells of a species foreign to the normal host species, i.e. a virus that is capable of growing in a foreign environment).
XMRV is a member of the same family of retroviruses as the AIDS virus. A retrovirus inserts itself into the host’s genetic material by copying its genetic code into the DNA of the host by using RNA and once there, it stays for the life of the host.
It is understood that Mikovits’ discovery was deemed to be of such magnitude by the world’s most prestigious science journal that the authors’ paper (which was submitted on 6th May 2009) was sent to three times the customary number of referees prior to acceptance and publication.
Shortly before the Mikovits et al paper was published, on 24th September 2009 the Whittemore Peterson Institute (WPI) announced that Dr Mikovits and collaborator Dr Jonathan Kerr of St George’s, London, had been awarded a $1.6 million five-year grant by the US National Institute of Allergy and Infectious Diseases for research into the causes and diagnosis of neuro-immune diseases (http://www.wpinstitute.org/news/news_current.html ). The Project Number is 1R01A1078234-01A2 and the description provided by the applicants says:
“CFS is a complex disease estimated to affect between 0.5% - 2% of the population of the Western world. Its pathogenesis is thought to involve both inherited and environmental (including viral) components, as with other chronic inflammatory diseases such as multiple sclerosis…Consistent with this chronic inflammatory context, CFS patients are known to have a shortened life-span and are at risk for developing lymphoma. We hypothesise that chronic inflammatory stimulation from active and recurrent infections of multiple viruses on a susceptible host genetic background leads to the pathogenesis characterised by CFS. The overall goal of this research project is to define those viral and host parameters…The proposed research will provide significant insight into the disease mechanism of Chronic Fatigue Syndrome so accurate testing and specific treatments can be developed with a goal of curing the disease and preventing life-threatening complications”
(Co-Cure NOT:RES:21st October 2009).
It is worth noting that three days before the Mikovits et al article was published in Science, on 5th October 2009 Professor Peter White in collaboration with Dr Bill Reeves of the CDC published a paper in which they described endophenotypes of CFS (which White talked about in his presentation at Bergen on 20th October 2009 – see below). According to Wikipedia,
“endophenotype” is a psychiatric concept, the purpose of which is to divide behavioural symptoms into separate phenotypes with clear genetic connections. The relevance of this to the neuro-immune disease ME/CFS has not been explained, but White and Reeves et al concluded: “The data do not support the current perception that CFS represents a unique homogeneous disease”
(Population Health Metrics 2009:7:17doi:10.1186/1478-7954-7-17).
In contrast, in their article in Science Mikovits et al deal with science, not speculation:
“Chronic fatigue syndrome (CFS) is a debilitating disease of unknown aetiology that is estimated to affect 17 million people worldwide.
“Studying peripheral blood mononuclear cells (PBMCs) from CFS patients, we identified DNA from a human gammaretrovirus (XMRV) in 68 of 101 patient (67%) compared to 8 of 218 (3.7%) healthy controls” (gammaretroviruses are known to cause cancer, immunological and neurological diseases in animals).
“Cell culture experiments revealed that patient-derived XMRV is infectious and that both cell-associated and cell-free transmission of the virus are possible”.
“CFS affects multiple organ systems in the body. Patients with CFS display abnormalities in immune system function, often including chronic activation of the innate immune system and a deficiency in natural killer (NK) cell activity. A number of viruses, including ubiquitous herpesviruses and enteroviruses have been implicated as possible environmental triggers of CFS. Patients with CFS often have active b herpesevirus infections, suggesting an underlying immune deficiency.
“The recent discovery of a gammaretrovirus, XMRV, in the tumour tissue of a subset of prostate cancer patients prompted us to test whether XMRV might be associated with CFS. Both of these disorders, XMRV-positive prostate cancer and CFS, have been linked to alterations in the antiviral enzyme RNase L” (RNase L is the terminal enzyme in the 2-5A synthetase/RNase L antiviral pathway in the immune system and it plays an essential role in the elimination of viral mRNA. Deregulation of this pathway in subsets of ME/CFS patients has been reported extensively in the scientific literature. In ME/CFS, a wide spectrum of cleavage of RNase L is observed, a phenomenon also seen in MS patients, and such altered RNase L activity profoundly affects cellular physiology, including apoptosis or programmed cell death – Dr Neil Abbot: Co-Cure RES:MED: 16th October 2009).
“Neurological maladies and immune dysfunction with inflammatory cytokine and chemokine up-regulation are some of the most commonly reported features associated with CFS…The presence of infectious XMRV in lymphocytes may account for some of these observations of altered immune responsiveness and neurological function in CFS patients.
“In summary, we have discovered a highly significant association between the XMRV retrovirus and CFS.
“This observation raises several important questions. Is XMRV infection a causal factor in the pathogenesis of CFS or a passenger virus in the immunosuppressed CFS patient population?…Conceivably these viruses could be co-factors in pathogenesis, as is the case for HIV-mediated disease, where co-infecting pathogens play an important role. Patients with CFS have an elevated risk of cancer.
“It is worth noting that 3.7% of the healthy donors in our study tested positive for XMRV sequences. This suggests that several million Americans may be infected with a retrovirus of as yet unknown pathogenic potential”.
Commenting on this further information, ME/CFS expert Dr Paul Cheney said:
On the day that the news broke of the XMRV link with ME/CFS, it was widely reported; prominent sources included AFP; Reuters; Wall Street Journal; Washington Post; New York Times; Nature; Scientific American; New Scientist; NIH News; Science News; NCI Press Release; Scientist, and many national newspapers such as the UK’s Daily Telegraph and The Independent. Numerous links can be found at http://bit.ly/13nShx.
The Wall Street Journal quoted Judy Mikovits as saying that the XMRV virus creates an underlying immune deficiency which might make people vulnerable to a range of diseases, and it continued:
AFP (Agence France Presse) quoted Mikovit’s co-author Francis Ruscetti of the Laboratory of Experimental Immunology at the National Cancer Institute:
Science News pointed out:
Mikovits found XMRV in a sample of frozen blood that had been saved by Dan Peterson as long ago as 1984. The blood happened to have been drawn from a patient who went on to die of mantle cell lymphoma, another disease XMRV is suspected of causing…the failure of the Centres for Disease Control to respond professionally and rationally when presented with a novel retrovirus in patients and their close contacts in 1991 by Elaine De Freitas needs to be revisited immediately…We’ve monitored the agency’s wilful ignorance of – indeed, their extreme hostility to – the science in this field….if it turns out that their failure to replicate Elaine de Freitas’ findings of a novel retrovirus in this disease, followed by their attempt to destroy her professional reputation, was purposeful, then…the CDC is as much a crime scene as it is a federal science agency.
How could our government and the governments of other nations dismiss and then ignore millions who suffered from ‘an infectious disease of the brain’ as Hilary Koprowski of the Wistar Institute called it publicly in 1992. Koprowski was an expert in neurological diseases – he knew one when he saw one…they will talk about the dangers of scientific bias and the near-criminal manner in which a disease could be defined, for so long and in spite of so much contrary evidence – as a personality disorder…The years of our lives during which thousands of research papers were written by psychiatrists purporting to explain away a life-destroying disease with discussions of personality disorders, exercise and activity phobia, malingering, hysteria, sexual abuse, school phobia, attention-seeking behaviour must be respected (and) the papers saved for posterity. Princeton English professor Elaine Showalter’s book equating this disease with fantasies of alien abduction probably deserves its own shelf in this pantheon of the grotesque…All these works will be examined, in time, by researchers who seek to understand the human capacity for delusion, ignorance and greed”
(http://www.oslersweb.com/blog.htm?post=638469 ).
Particularly notable was the BBC’s reporting of the comments of Tony Britton, the (lay) Publicity Manager at the UK ME Association: “This is fascinating work, but it doesn’t conclusively prove a link between the XMRV virus and chronic fatigue syndrome or ME”, a statement that should be compared with what was published in Science: “we have discovered a highly significant association between the XMRV retrovirus and CFS” and with the WPI press release: “This finding clearly points to the retrovirus as a significant contributing factor in this illness”.
It is regrettable that the UK ME Association’s Publicity Manager seems not to distinguish between proving a conclusive cause and proving a direct link, a link that certainly satisfied the many prestigious referees who advised the journal Science.
It also satisfied Richard T Ellison III, Professor of Medicine, Molecular Genetics and Microbiology in the Division of Infectious Diseases and Immunology at the University of Massachusetts Medical School (Deputy Editor of Journal Watch Infectious Diseases since 1988), who commented:
“These studies provide clear evidence that active XMRV infection occurs in many CFS patients” (Co-Cure RES: 22nd October 2009).
Moreover, as Hillary Johnson reported in the New York Times on 21st October 2009, Judy Mikovits had worked for the National Cancer Institute for 22 years and she was impressed that Dan Peterson
“had built an extraordinary repository of more than 8,000 chronic fatigue syndrome tissue samples going back as far as 1984…What (Mikovits) found was live, or replicating, XMRV in both frozen and fresh blood and plasma, as well as saliva. She has found the virus in samples going back to 1984 and in nearly all the patients who developed cancer. She expects the positivity rate will be close to 100% in the disease. ‘It’s amazing to me that anyone could look at these patients and not see that this is an infectious disease that has ruined lives,’ Dr Mikovits said. She has also given the disease a properly scientific new name: X-associated neuroimmune disease (XAND)”.
On 20th October 2009 Judy Mikovits herself was interviewed; she said:
“John Coffin is a member of the US National Academy of Sciences. No greater authority on these viruses exists. Three members of the US National Academy of Sciences reviewed this work and all are convinced of the science…they are convinced of the infection and the public health risk”
(http://merutt.wordpress.com/tag/chronic-fatigue-syndrome/ ).
Interviewed live by Rene Montagne, when asked why people thought sufferers don’t really have a disease, Dr Daniel Peterson, medical director of the WPI, was clear:
“I think the reason for that is the abnormalities of the immune system are initially very subtle. And if a physician does just routine testing – you find they’re normal. It isn’t until you look at the immune system that you realise there’s substantial dysregulation…It’s very similar to asymptomatic carriers of HIV. They look just fine until time passes and their illness evolves and more symptoms are found. But I never felt this was predominantly a psychiatric disease or malingering. There was never any evidence to support that theory…Once it was demonstrated that the patients had impairment of the natural killer cells function, regardless of what country they were in, we knew that there was immune impairment…Back in the 1990s, I was associated with Temple University and researchers (who) looked at the antiviral pathway…found very substantial abnormalities in the patients who had chronic fatigue syndrome. And the illness is totally compatible with a viral illness that just doesn’t go away”
(http://www.npr.org/templates/story/story.php?storyId=113650222 ).
Following the (re)discovery of a direct link between a retrovirus and ME/CFS, there has been much internet traffic about the dismissing and ignoring by US agencies of state of Dr De Freitas et al’s work two decades ago that demonstrated a potential retroviral link, particularly in relation to possible transmission via blood products.
This down-playing has been ascribed by some people to (i) a possible UK/US collaboration over the use of biowarfare agents, including borrelia (“US Government Admits Lyme Disease Is A Bioweapon”: Co-Cure ACT: 1st January 2006: http://www.indymedia.org.uk/en/2005/11/328067.html and http://www.lyme-rage.info/elena/statejun06.html); (ii) the CDC’s apparent determination to prevent at any cost public panic over the emergence of another AIDS-like pandemic and (iii) the wish to protect insurers from having to make payments for another chronic disease, factors that may be instrumental in Dr Bill Reeves’ dismissive comments about the latest discovery of an association between a retrovirus and ME/CFS:
Against this background, there are mounting calls for the removal of Dr Reeves from his position as principal investigator of the CDC’s CFS research programme (“Support the 500 Professionals of the IACFS/ME – Reeves Must Go”):
“On May 27th and May 28th, 2009, the Chronic Fatigue Syndrome Advisory Committee (CFSAC) convened in Washington, D.C. Among their recommendations to the Secretary of Health and Human Services was a call for new and progressive leadership at the CDC's ME/CFS research division. Under Bill Reeves' regime, funding has routinely decreased and increasingly broad definitions which have ceased to have any clinical meaning or research value have been implemented…. Under Reeves' direction the CFS program is being slowly strangled…. What does Reeves say about Mikovits’ recent discovery? Without doing any study or due diligence, Reeves dismisses the findings… Inaccurate stereotypes persist because Bill Reeves has not been accurately educating the public on the seriousness of this disease”
(Co-Cure ACT: 25th October 2009).
Comments such as that by Tom Kindlon from the Irish ME/CFS Association reflect the position of many in the international ME/CFS community:
“What does he mean ‘much less an illness like CFS’? CFS is much more like a chronic viral disease than most chronic diseases. Why is he heading a programme based in the viral section of the CDC if he has this attitude?”
(Co-Cure ACT:8th October 2009).
In her customary robust manner, Hillary Johnson in the US is scathing about Bill Reeves:
Notably, Dr Stuart Le Grice, head of the Centre of Excellence in HIV/AIDS and cancer virology at the National Cancer Institute went on record saying:
“NCI is responding like it did in the early days of HIV” (in other words, by dismissal and denial of the significance). As Cort Johnson observed: “Neither the CDC nor the NIH (with the exception of NK cells) have shown any interest in pathogens of the immune system in over ten years. Research into ME/CFS has declined precipitously in both institutions over the past five years”
(http://aboutmecfs.org/blog/?p=920 )
In response to an article in Nature by Lizzie Buchen who quoted Judy Mikovits as saying:
In the UK, Simon Wessely is similarly unpopular, and for similarly well-founded reasons.
On 5th February 1999 that the New Statesman carried an article by Ziauddin Sardar about Wessely (titled “Ill-defined notions”) in which Sardar wrote:
“The same can be said of Gulf War syndrome.…again, there are lots of nasty symptoms: mild to moderate chronic fatigue, double vision, severe urinary and sexual problems, memory loss, joint and muscular pain — to start with…But even though 400 veterans have actually died and some 5,000 are suffering from illnesses related to Gulf War syndrome, the syndrome does not officially exist.
“All the actors involved in this drama have their own perspective... .the government with avoiding paying compensation at all costs. So one would expect the Ministry of Defence to deny the existence of Gulf Way syndrome and it does, operating on the simple basis of “no bug, no dosh”.
“...this makes life very hard for sufferers. They not only have to survive their disease: they must also fight for elementary decency. And that is a long and bitter task in itself.
“But what of researchers? Why should they deny the existence of Gulf War syndrome? The struggle over recognition hinges on research. But this research is a totally different exercise...How do you investigate this mess of symptoms? Not with biochemistry, but with psychiatry.
“The new societal syndrome of syndromatic diseases requires a new speciality, a syndromologist. Fortunately, one is to hand. His name is Professor Simon Wessely, consultant psychiatrist at the School of Medicine, King’s College, London.
“Wessely has been arguing that ME is a largely self-induced ailment that can be cured by the exercise programme on offer at his clinic.
“Recently he published the results of “the most definitive study” of Gulf War syndrome in.. .the Lancet... .It concluded — surprise, surprise — that there is no such thing as Gulf Way syndrome.
“So Wessely, who occupies a key position in our socio-medical order, denies the existence of Gulf War syndrome, just as he denies the existence of ME.
“Clearly, he is a follower of Groucho Marx: ‘Whatever it is, I deny it’. Not surprisingly, lots of people hate him.
“If Simon Wessely is our syndromologist-in-chief, who has chosen and vetted him for that post, and by what criteria and procedures? Where is the debate over the shaping of such research?…When will we have the first officially sponsored study of such a problem which the sufferers do not have the occasion to call a whitewash?”.
Since at least 1994, when the CFIDS Chronicle published an article titled “The views of Dr Simon Wessely on ME: Scientific Misconduct in the Selection and Presentation of Available Evidence” (Spring 1994:14-18), valid criticisms of Wessely have continued to mount, some of which can be accessed at http://www.meactionuk.org.uk.
In his article in New Scientist on 9th October 2009 (referred to above), Ewen Callaway noted Professor Wessely’s position regarding the discovery of XMRV in CFS patients:
“Wessely points out that XMRV fails to account for the wide variety of other factors associated with the CFS, including childhood trauma…’Any model that is going to be satisfactory has to explain everything, not just little bits’ he says”.
Wessely’s belief that childhood trauma causes ME/CFS takes no account of those who had a happy, secure childhood within a stable and loving family but who still developed severe ME/CFS.
Similar points are reflected in the many online comments posted to the New Scientist. These were highly critical of Wessely’s dismissive attitude, and provided examples of the adverse impact on patients of his ill-grounded beliefs about ME/CFS, for example:
“Dr Wessely had the chance to prove he had some kind of humility with regard to his disgraceful behaviour towards ‘CFS’ ”
“Now if that’s not the sound of a desperate drowning man clinging to the sinking wreckage of his fatally flawed theory for ME. Give it up, Wessely, sink to the bottom of the sea, vanish without trace. The time has come once and for all to banish these primitive psychological theories to the dustbin of medical history, where they so rightfully belong”
“Completely agreed – Simon Wessely, the medical establishment and local authorities that have taken children into care, sectioned adults, forced harmful treatment, ruined lives, should be made to apologise to every single one of their victims, not only here but worldwide”
“Holding a different evidence-based view-point is one thing – ignoring evidence and letting ego condemn patients to grotesque suffering and death as a physician is evil and should be dealt with as such”
“I look forward to seeing the psychological research by Professor Wessely published in the journal Science”
“I was diagnosed with ME in 1992 –3.. …I’m a former clinical specialist in life-support technology, qualified in medicine, perfusion science and life-support technology, so I know a bit about all this. I empathise with anyone who has genuinely suffered this condition, especially when they have not had good treatment from their own doctors”
“To the Editor: It remains a mystery as to why you bother including the unsubstantiated opinion provided by Dr Simon Wessely. He continues to profit from the prescription of cognitive therapy for this serious illness, despite the fact that the majority of patients fail to benefit from such interventions. By any other model, insistence upon cognitive therapy as the default model for treatment should constitute malpractice”
“I saw on my doctor’s notes that the symptoms were all in my ‘mind’. This was despite a low white cell count, inflamed spleen and swollen lymph nodes. Yep, the low white cell count was because of my ‘mind’. If they dismissed cancer this way the overpaid morons would be sued for malpractice;
“Those physicians may have some red-faced explaining to do if this research pans out”
“ ’Red-faced’ – no, they should be sued for negligence. Sorry, but I was damn near killed by such idiocy so I have not the slightest sympathy for such bigoted physicians…I want several prominent persons responsible for this terrible abuse of millions of ill people across the globe criminally charged and tried for negligence…Many people have DIED because of this, either by direct abuse by doctors, or by disdainful refusal to aid, or actively preventing research into physical causes. Sophia Mirza is only one such victim, most others just sank without trace as it was ‘inconvenient’ and their death or suicides were ‘all their own fault as it was all in their heads’. But when a physician deliberately ignores his duties because of prejudice – that, sir, is ABUSE. Imagine how an MS sufferer would feel if they were ignored, abused, even sectioned by the very physician who swore an oath to help them. And then the very person at the top of the pyramid of abuse was allowed to publish articles about MS…”
”But, Simon, you said they thought themselves sick…Wessely points out that XMRV fails to account for the wide variety of other factors associated with the CFS, including childhood trauma….but Professor Wessely was quite happy to lead nations to think that these unfortunate people were all suffering from ‘abnormal illness beliefs’. Why was he so happy to ignore biomedical research which demonstrated that this disease was not a mental illness?”
“Simon Wessely…(has) a lot to answer for…I have yet to meet someone with ME who hasn’t inspired me with their strength. It’s just a shame there is so much to fight against”
“The idea that ME was somehow linked to childhood trauma was always nonsense…Way back when I was first ill, researchers were looking for a retrovirus. The problem was that no-one would fund them and allow then to continue their work. They were repeatedly turned down and their work blocked. This retrovirus should have been discovered at the same time as AIDS and the last few miserable decades of my life could have been avoided…No more excuses and no more psychobabble”
“Tragically for sufferers, the psychological zealots are ruling the asylum and they have steered successive definitions away from viral, inflammatory disease and to their beloved ‘unexplained fatigue’ and disingenuous ‘psychological factors’. Mediocre findings of CBT/GET have been spun more than a New Labour carousel leading a character assassination on the ME community, creating an ideological distortion of the very presentation of the disease, whereby misled doctors dismiss such unfortunate patients as ‘pond life’ or ‘ME lunatics’ and deny even the most severely affected (eg bedbound) patients access to investigation, treatments, monitoring, advocacy and education of social and welfare support networks, while taking no interest in/dismissing the literature themselves. Cue great neglect, suffering, exploitation, wasted generations and premature deaths. Will the psych/med profession apologise? Just as with past outrages against multiple sclerosis (and) Parkinsons, will they hell”
(http://tinyurl.com/yl55so8)
Other similar comments about Wessely were posted in response to The Independent’s coverage of the XMRV discovery, for example:
On other sites (for example; http://www.meactionuk.org.uk/wessely.html), people recalled what Wessely has said and published about ME/CFS in the past, for example:
“What lies behind all this talk of viruses and immunity?…..Talk of viruses and the immune system is now embedded in popular consciousness….Viruses are an attribution free from blame…there’s no blame, no shame and no stigma….And (mocking) here is the virus research doctor himself to protect us from that shame….And what is it he delivers? Respect” (Microbes, Mental Illness, the Media and ME: The Construction of Disease. 9th Eliot Slater Memorial Lecture, Institute of Psychiatry, 12th May 1994).
“Wessely sees viral attribution as somatisation par excellence” (Helen Cope, Anthony David, Anthony Mann. Journal of Psychosomatic Research 1994:38:2:89-98).
In a reply to someone who wrote to him on 12th November 2009 asking for his response to the XMRV findings, Wessely replied:
“Could be a real breakthrough, even if I still don’t understand how they made the leap from prostate cancer to CFS”, which seems to indicate that Wessely remains ignorant of or else does not understand what Judy Mikovits et al said: “both are linked to alterations in the antiviral enzyme RNase L”, a link that was clearly explained by David Bell in his Lyndonville News, volume 6, number 2, October 2009:
"XMRV was first linked to human disease by Robert H Silverman, PhD at the Cleveland Clinic in patients with prostate cancer who also had a defect in the RNAse L antiviral pathway. As this pathway has been known to be abnormal in CFS, it was reasonable to search for the virus in CFS". Wessely then seemed to deny the association with XMRV and cancer: “I am worried that 20% of the CFS patients seem to have lymphoma (ie cancer), which might be fascinating for our knowledge of cancer but really isn’t relevant for CFS”. Apparently adopting the same stance as Bill Reeves in the US, Wessely continued: “I would be very surprised indeed if others find rates of XMRV at the same level as this paper”
(Co-Cure ACT: 12th November 2009).
There is international recognition that Wessely
An internet search will quickly reveal that there is extensive outrage about Simon Wessely and his colleagues’ unproven beliefs, not only from ME/CFS patients and their long-suffering families, but also from international medical scientists and clinicians who are not blinded by ideology or vested interests.
In his article in The Independent on 9th October 2009 (referred to above), Steve Connor also quoted Professor Simon Wessely’s views on the implications of the XMRV discovery:
On 29th October 2009 Professor Coffin told a Department of Health and Human Services Committee that this discovery was of “potentially extraordinary importance”, not least, as Jack Johnson reported (Co-Cure NOT:16th November 2009), because it means validation and hope for millions of people suffering from (ME)CFS, often thought by many to be nothing more than the product of neurosis and even laziness and, as Jack Johnson pointed out: “CFS has long been thought to be linked to retroviral infection”.
As noted in “Denigration by Design? A Review, with References, of the Role of Dr (now Professor) Simon Wessely in the Perception of Myalgic Encephalomyelitis (Up-date) Volume II (http://www.25megroup.org/denigration%20by%20design/denigration%20contents.htm), it seems that to Wessely and his closest associates, the belief of the moment represents the only truth.
They would do well to remember that in the early 1600s, King James I of England (who was also King James VI of Scotland) wrote a book called “Demonology” and that book helped to send to their death women known as the Lancashire witches. Countless innocent women were persecuted, tortured and executed as witches, having been forced into admitting things they did not do, the majority being people who suffered from mental illness.
Incredibly, it was not until the 1950s that the Witchcraft Act was repealed in the UK. This must surely serve as a salutary reminder that the belief of the time (currently, that ME/CFS is a behavioural disorder) is not necessarily the truth, even though it might be promoted as the truth.
It is fair to say that the views of Wessely and his close colleagues (including those involved with the PACE Trial) are held in contempt by many people – medical and lay alike – who have to deal with the reality and severity of ME/CFS, yet injustice for those with ME/CFS continues. Cases of untold suffering and despair continue to accumulate, and this is very significantly because of the influence of the Wessely School.
One can but pray that along with his colleagues Peter White, Michael Sharpe and Trudie Chalder, Wessely’s power and influence – unlike that of demonology – will not remain enshrined for the next 350 years and that medical science may at last have provided the means to right the wrongs that the Wessely School have done so much to perpetrate upon those with ME/CFS.
That such wrongs exist in the US is further demonstrated by the testimony of Kenneth Friedman on 30th October 2009 before the CFS Advisory Committee (Co-Cure NOT:MED: 4th November 2009). Friedman, a medical school professor at the Department of Pharmacology and Physiology, New Jersey Medical School, said:
“I have been asked to comment upon the status of Chronic Fatigue Syndrome education in the United States.
“The Director of the Office of Ethics and Compliance has informed me that my off-campus activities relating to CFS which include testifying before this Committee, serving on this Committee, providing continuing medical education courses, establishing medical student scholarships and assisting with healthcare legislation are not part of my responsibilities as a University Professor.
“ I am told that I will be punished with a penalty as severe as termination of my employment for these activities.
“I am not a unique target. Colleague Ben Natelson (an ME/CFS researcher who was Professor in the Department of Neurosciences at New Jersey Medical School) has left the same school.
“A different medical school has refused to permit access to their medical students to discuss CFS.
“A statewide healthcare provider…refuses to permit a CFS training session for their physicians.
“The failure of the CDC to convince the medical-academic establishment of the legitimacy of CFS, and the urgent need for its treatment, has created this environment”.
Could it be said that the Wessely School has created a similar environment in the UK and that the MRC PACE Trial is part of that constructed environment, just as the NICE Clinical Guideline and the actions of NICE which resulted in the failure of the Judicial Review were also part of it?
1954: Encephalomyelitis associated with poliomyelitis virus. ED Acheson. Lancet: Nov 20th 1954:1044-1048.
1955: Outbreak at The Royal Free. ED Acheson. Lancet: Aug 20th 1955:394-395.
1959: The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia. ED Acheson. American Journal of Medicine, April 1959:569-595. (Note that neuromyasthenia is not the same as neurasthenia).
1978: An outbreak of encephalomyelitis in the Royal Free Hospital Group, London, in 1955. Nigel D Compston. Postgraduate Medical Journal 1978:54:722-724.
1983: Sporadic myalgic encephalomyelitis in a rural practice. BD Keighley, EJ Bell. JRCP 1983:33:339-341.
1985: Characteristic T cell dysfunction in patients with chronic active Epstein-Barr virus infection. G Tosato, S Straus et al. The Journal of Immunology 1985:134:5:3082-3088. (Note that what is now called ME/CFS was then thought to be caused by EBV).
1985: Persisting Illness and Fatigue in Adults with Evidence of Epstein-Barr Virus Infection. Stephen E Straus et al. Ann Intern Med. 1985:102:7-16.
1985: The postviral fatigue syndrome – an analysis of the findings in 50 cases. PO Behan, WMH Behan, EJ Bell. Journal of Infection 1985:10:211-222.
1987: Post-Viral Fatigue Syndrome. TJ Marrie et al. Clinical Ecology 1987:V:1:5-10.
1987: Coxsackie B viruses and the post-viral syndrome: a prospective study in general practice. BD Calder et al. JRCGP 1987:37:11-14.
1987: The Epstein-Barr Virus and Chronic Fatigue. Irving E Salit. Clinical Ecology 1987:V:3:103-107.
1988: Chronic enterovirus infection in patients with Postviral Fatigue Syndrome. GE Yousef, EJ Bell, JF Mowbray et al. Lancet January 23rd 1988:146-150.
1988: Chronic fatigue syndromes: relationship to chronic viral infection. Anthony L Komaroff. Journal of Virological Methods. 1988:21:3-10.
1988: Postviral Fatigue Syndrome. PO Behan, WMH Behan. CRC Crit Rev Neurobiol 1988:4:2:157-178.
1988: Transmissible disease and psychiatry. Magnetic resonance muscle studies; implications for psychiatry. RP Yonge. JRSM 1988:81:322-326.
1988: Human enteroviral infections. EG Dowsett. Journal of Hospital Infection 1988:11:103-115.
1990: 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. L Cunningham, RJM Lane, LC Archard et al. Journal of General Virology 1990:71:6:1399-1402.
1990: Myalgic encephalomyelitis – a persistent enteroviral infection? EG Dowsett, AM Ramsay et al. Postgraduate Medical Journal 1990:66:526-530.
1991: Retroviral sequences related to human T-lymphotropic virus type II in patients with chronic fatigue immune dysfunction syndrome. Elaine De Freitas, Paul R Cheney, David S Bell et al. Proc Natl Acad Sci USA 1991:88:2922-2926.
1991: Enteroviral RNA sequences detected by polymerase chain reaction in muscles of patients with postviral fatigue syndrome. JW Gow et al. BMJ 1991:302:696-696.
1991: Considerations in the Design of Studies of Chronic Fatigue Syndrome. Reviews of Infectious Diseases. Volume 13, Supplement 1: S1 – S140. University of Chicago Press. Contributing authors include: S. Grufferman, AL Komaroff, DS Bell, DL Peterson, S Daugherty, S Bastien.
1991: Postviral Fatigue Syndrome. British Medical Bulletin 1991:47:4: 793-907. Churchill Livingstone.
1993: Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy. NE Bowles et al. Journal of Medicine 1993:24: 2&3:145-180.
1993: Enteroviruses and postviral fatigue syndrome. PO Behan, JW Gow et al. CFS: CIBA Foundation Symposium: 1993: 146-159.
1994: Changes in the 2-5A Synthetase/RNase L Antiviral Pathway in a Controlled Clinical Trial with Poly(I)-Poly (C12U) in Chronic Fatigue Syndrome. Robert J Suhadolnik, Daniel L Peterson, Paul Cheney et al. In Vivo 1994:8:599-604.
1994: Chronic Fatigue Syndrome: Current Concepts. Clinical Infectious Diseases 1994: Volume 18: Supplement 1: S1 – S167. Ed. Paul H Levine. University of Chicago Press. Contributing authors include: Paul H Levine, Alexis Shelokov, Anthony L Komaroff, David S Bell, Paul R Cheney, Leonard H Calabrese, Leonard A Jason, Seymour Grufferman, Hirohiko Kuratsune, Charles Bombadier, Nancy G Klimas, Mary Ann Fletcher, Roberto Patarca-Montero, Benjamin H Natelson, Robert J Suhadolnik, Daniel L Peterson, Dharam V Ablashi, Fred Friedberg, Jay A Levy, Peter O Behan, Wilhelmina MH Behan and Mark O Loveless.
1995: Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome. DN Galbraith et al. Journal of General Virology 1995:76:1701-1707.
1995: Comparison of Coxsackie B Neutralisation and Enteroviral PCR in Chronic Fatigue Patients. C Nairn et al. Journal of Medical Virology 1995:46:310-313.
1995: Detection of Enterovirus-Specific RNA in Serum: The Relationship to Chronic Fatigue. GB Clements et al. Journal of Medical Virology 1995:45:156-161.
1997: Evidence for enteroviral persistence in humans (with CFS). DN Galbraith et al. Journal of General Virology 1997:78:307-312.
1997: Biochemical evidence for a novel low molecular weight 2-5A-dependent RNaseL in chronic fatigue syndrome. Suhadolnik RJ, Peterson DL et al. J Interferon Cytokine Res 1997:17(7):377-385.
1998: Enteroviral Infections and their Sequelae. EG Dowsett. BSAEM; RCGP 1998:1-10.
2000: Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. DV Ablashi, DL Peterson et al. Journal of Clinical Virology 2000:16:179-191.
2001: Viral Isolation from Brain in Myalgic Encephalomyelitis (A Case Report). J Richardson. JCFS 2001:9:3/4:15-19.
2001: Enterovirus in Chronic Fatigue Syndrome. N-T Jou et al. Arthritis & Rheumatism 2001:44:S9:S351.
2001: Prevalence in the Cerebrospinal Fluid of the Following Infectious Agents in a Cohort of 12 CFS Subjects: Human Herpes Virus-6 and 8; Chalmydia Species; Mycoplasma Species, EBV; CMV and Coxsackievirus. Susan Levine. JCFS 2002:9:1/2:41-51.
2001: Dynamics of chronic active herpesvirus-6 infection in patients with chronic fatigue syndrome. Krueger GR et al. In Vivo 2001:15(6):461-465.
2001: G-Actin Cleavage Parallels 2-5A-Dependent RNase L Cleavage in Peripheral Blood Mononuclear Cells – Relevance to a Possible Serum-Based Screening Test for Dysregulations in the 2-5A Pathway. S Roelens, P Englebienne et al. JCFS 2001:8:3/4:63-82.
2002: Antiviral Pathway Activation in Chronic Fatigue Syndrome and Acute Infection. Kenny De Meirleir, Robert J Suhadolnik et al. Clinical Infectious Diseases 2002:34:1420-1421.
2002: Structural and Functional Features of the 37-kDa 2-5A-Dependent RNase L in Chronic Fatigue Syndrome. Shetzline SE, De Meirleir K, Peterson DL et al. J Interferon Cytokine Res 2002:22(4):443-456.
2002: The Paul-Bunnell Heterophile Antibody Determinant in Epstein-Barr Virus-Associated Disease. Roberto Patarca-Montero and Mary Ann Fletcher. JCFS 2002:10:3/4:51-86.
2002: Ribonuclease L Proteolysis in Peripheral Blood Mononuclear Cells of Chronic Fatigue Syndrome Patients. Edith Demettre, Kenny De Meirleir, Patrick Englebienne et al. Journal of Biological Chemistry 2002:277:38:35746-35751.
2003: Multiple co-infections (Mycoplasma, Chlamydia, HHV-6) in blood of chronic fatigue syndrome patients: association with signs and symptoms. Nicolson GL et al. APMIS 2003:111(5):557-566.
2003: Enterovirus related metabolic myopathy: a postviral fatigue syndrome. RJM Lane, LC Archard et al. JNNP 2003:74:1382-1386.
2003: Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease in fibromyalgia and healthy subjects. Douche-Aourik F et al. Journal of Medical virology 2003:71:540-547.
2005: Assessment and Implications of Viruses in Debilitating Fatigue in CFS and MS Patients. Dharam V Ablashi et al. HHV-6 Foundation, Santa Barbara, USA. Submission to Assembly Committee/Ways & Means, Exhibit B1-20, submitted by Annette Whittemore 1st June 2005.
2005: The role of enterovirus in chronic fatigue syndrome. JKS Chia. Journal of Clinical Pathology 2005:58:1126-1132.
2006: Chronic Fatigue Syndrome. LD Devanur, JR Kerr. Journal of Clinical Virology 2006: 37(3):139-150.
2006: Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study. Ian Hickie et al. BMJ 2006: 333:575.
2006: Antiviral Pathway Deregulation of Chronic Fatigue Syndrome Induces Nitric Oxide Production in Immune Cells that Precludes a Resolution of the Inflammatory Response. Marc Fremont, Kenny De Meirleir et al. JCFS 2006:13:4:17-28.
2006: Is HHV-6 a trigger for chronic fatigue syndrome? Anthony L Komaroff. Journal of Clinical Virology 2006:37:S1:S39-S46.
2007: Chronic Fatigue Syndrome is associated with chronic enterovirus infection of the stomach. Chia JK, Chia AY. J Clin Pathol 13th September 2007 Epub ahead of print.
2007: Enterovirus infection of the stomach in Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME). Jonathan R Kerr. Editorial. J Clin Pathol 14th September 2007. Epub ahead of print.
2008: 5' terminal deletions in the genome of a coxsackievirus B2 strain occurred naturally in human heart. Virology 2008 Jun 5;375(2):480-91.
2009: Human Enteroviruses and Chronic Infectious Disease. S Tracy and NM Chapman. Journal of IiME 2009:3:1 (http://www.investinme.org/Documents/Journals/Journal%20of%20IiME%20Vol%203%20Issue%201.pdf).
References: The role of viruses in ME/CFS – some illustrations from the literature
