Showing posts with label XMRV. Show all posts

Wednesday, May 23, 2012

Novel MLV-GAG sequences detected in blood samples of ME/CFS patients

Dr. O'Keefe: From the Hanson lab, this paper published today in PLoS ONE describes a study carried out with meticulous attention to detail and proper use of controls while analyzing ME/CFS patient samples for murine-leukemia related viruses. Although novel MLV-like GAG sequences were isolated and sequenced from the patient samples (as opposed to controls collected from the same sites) Lee et al. concludes that it is not possible to determine the origin of these sequences, although the samples were not contaminated with mouse DNA at a detectable level.

First, bravo! to the Hanson group for being able to get anything published that might go against the current dogma regarding MLV-like viruses in human samples published -- I guarantee you that there are people with similar data whom don't want to torture themselves by attempting to publish. The fact is, Read more>>

Saturday, February 18, 2012

British Journal of Cancer February 2012: involvement of XMRV in the pathogenesis of MCC and prostate carcinomas remains unclear

British Journal of Cancer , (16 February 2012) | doi:10.1038/bjc.2012.51

http://www.nature.com/bjc/journal/vaop/ncurrent/full/bjc201251a.html

No evidence for the involvement of XMRV or MCV in the pathogenesis of breast cancer

G Khan, P S Philip, M Naase and K M I Al Zarouni

Abstract
Background:

The aetiology of breast cancer remains elusive. A viral aetiology has been proposed, but to date no virus has been conclusively demonstrated to be involved. Recently, two new viruses, namely Merkel cell polyomavirus (MCV) and xenotropic murine leukaemia virus-related virus (XMRV) have been identified and implicated in the pathogenesis of Merkel cell carcinoma (MCC) and familial form of prostate cancer, respectively.

Methods:

We examined 204 samples from 58 different cases of breast cancer for presence of MCV or XMRV by PCR. Samples consisted of both malignant and non-malignant tissues. Additionally, we included 6 cases of MCC and 12 cases of prostate cancer as potential controls for MCV and XMRV, respectively.

Results:

All of the breast cancer samples examined were negative for both MCV and XMRV. However, 4/6 MCC and 2/12 prostate cancer samples were found to be positive for MCV and XMRV, respectively. Sequence analysis of the amplified products confirmed that these sequences belonged to MCV and XMRV.

Conclusion:

We conclude that there is no evidence for the involvement of MCV or XMRV in the pathogenesis of breast cancer. What role these viruses have in the pathogenesis of MCC and prostate carcinomas remains to be demonstrated.

Tuesday, February 7, 2012

Experts now generally believe that infectious agents set off a persistent, hyperactive immune response that causes chronic fatigue syndrome

By DAVID TULLER Published: February 6, 2012: An estimated one million people in the United States suffer from chronic fatigue syndrome, which is characterized by profound exhaustion, a prolonged loss of energy following minimal exertion, swollen lymph nodes, sore throat, cognitive dysfunction and other symptoms. Experts now generally believe that one or more infectious agents, or perhaps exposure to toxins, set off a persistent, hyperactive immune response — the likely cause of many of the symptoms.

¶ The events of the past couple of years, though disheartening to chronic fatigue syndrome patients, may have a silver lining: Research into the disease, much of it privately financed, is ratcheting up.

¶ A new research and treatment center has been created at Mount Sinai Hospital in New York. The Hutchins Family Foundation is investing $10 million in the Chronic Fatigue Initiative, an effort to find causes and treatments that has recruited top researchers from Columbia, Harvard, Duke and other institutions.

¶ “The disease had languished in the background at N.I.H. and C.D.C., and other scientists had not been paying much attention to it,” said John Coffin, a professor of molecular biology at Tufts University. “This has brought it back into attention.”

¶ Dr. Coffin, who at first supported the mouse retrovirus theory but later disputed it, noted that the illness “does seem to have characteristics that would suggest infectious origins” and that other retroviruses could be involved.

¶ Despite the personal and professional setbacks for Dr. Mikovits, many patients, like Ms. Solomon, continue to believe that a retrovirus is causing their illness.

¶ “But even if the retroviral research does not pan out, her work, and the publicity it has brought to our illness, has forever changed the landscape,” said Ms. Solomon.

Read more>>

Thursday, January 12, 2012

Prof Racaniello: the CDC has stumbled when tackling CFS, dismissing evidence that CFS is an organic disease, diverting funds designated for CFS to other programs

January 12th, 2012, by Vincent Racaniello, discovermagazine.com:

Vincent Racaniello is Higgins Professor of Microbiology & Immunology at Columbia University, where he oversees research on viruses that cause common colds and poliomyelitis. He teaches virology to graduate, medical, dental, and nursing students, and writes about viruses atvirology.ws.

The detection of a new virus called XMRV in the blood of patients with chronic fatigue syndrome(CFS) in 2009 raised hope that a long-sought cause of the disease, whose central characteristic is extreme tiredness that lasts for at least six months, had been finally found. But that hypothesis hasdramatically fallen apart in recent months. Its public demise brings to mind an instance when a virus *was* successfully determined to be behind a mysterious scourge: the case of HIV and AIDS. How are these two diseases different—how was it that stringent lab tests and epidemiology ruled one of these viruses out, and one of them in?

The first inklings of the disease now called AIDS surfaced in Los Angeles in the summer of 1981. The5 June 1981 issue of Morbidity and Mortality Weekly Report described 5 homosexual men withPneumocystis carinii pneumonia (abbreviated PCP), normally only observed in individuals with weakened immune systems. The article suggested the possibility of an immune dysfunction related to exposure to something that would make individuals vulnerable to opportunistic infections. Soon clusters of PCP and Kaposi’s sarcoma, a rare skin cancer, were observed in gay men in other urban centers. The Centers for Disease Control and Prevention established a simple case definition—Kaposi’s sarcoma or opportunistic infections—and began scouring hospital records. Over time this definition was modified, but its early use identified an ongoing epidemic, and identified groups at risk for the disease as men who have sex with men and injection drug users.

The next year the new disease was called AIDS, and soon the U.S. Public Health Service recommended that members of risk groups not donate blood or plasma. Soon came reports that the disease could be acquired by newborn babies from their mothers, and also by heterosexual contact. By the fall there were nearly 700 people who had been diagnosed with AIDS in the U.S., of whom almost 300 had died. The CDC and World Health Organization worked together to publish global data on the disease, and issue recommendations to prevent its spread.

During the early years, the epidemiology of AIDS suggested an infectious cause, and in 1983, just two years after the disease was identified, a novel retrovirus was isolated from a patient at risk for AIDS. A year later a commercial blood test was developed, which allowed comprehensive studies to be done that showed clearly that the virus, later named human immunodeficiency virus type I (HIV-1), was the cause of AIDS. This conclusion was strengthened by the transmission of AIDS to hospital workers when they inoculated themselves with HIV-containing blood by accidental needle sticks.

HIV (green) budding from an infected cell.

By 1987 the first anti-HIV drug, azidothymidine or AZT, was licensed for the treatment of AIDS. Today over 20 anti-HIV drugs have been approved. When given in combinations of three, the emergence of drug-resistant viral variants is minimized, transforming AIDS from a death sentence to a life-long chronic disease.

The story of CFS, generally defined as persistent fatigue of six months or greater not relieved by rest and accompanied by other specific symptoms, is markedly different. This syndrome was first reported in Los Angeles as well, but in 1934. There were subsequent sporadic outbreaks, some of which were reviewed by DA Henderson in 1959, who noted that females were more frequently affected, and suggested that a virus might be involved. In the 1980s Daniel Peterson identified antibodies against Epstein-Barr virus (EBV) in the blood of a group of CFS patients in Incline Village, Nevada. The CDC entered the investigation but was unable to confirm that antibodies to the virus were consistently present in patient blood. A subsequent case-control study failed to identify EBV as the causative agent of the disease, which was subsequently named chronic fatigue syndrome.

The search for that agent of CFS has continued to be fruitless. In addition to EBV, a host of other viruses have been found in CFS patients, including enteroviruses, measles virus, herpesviruses, and human T-lymphotropic virus type II. However, none have been consistently detected in CFS patients and therefore are not considered to cause the disease.

The possibility of a viral cause of CFS re-emerged in 2009 with the detection of a retrovirus called XMRV in the blood of a substantial fraction of CFS patients. A second laboratory subsequently identified sequences related to murine leukemia viruses, also retroviruses, in the blood of CFS patients. However, many other laboratories were unable to replicate these findings, and both papers have been retracted.

Why do the stories of AIDS and CFS have such different outcomes? One reason is that it has been difficult to reach a consensus on a clinical definition of CFS. At the onset the case definition of AIDS was simple—“Kaposi’s sarcoma or opportunistic infections”—which made it possible to rapidly and accurately identify new cases, especially among different research groups around the country. This led to the establishment of risk factors, and the epidemiological data obtained from this work made it highly likely that an infectious agent was involved, spurring the search for the causative pathogen. The case definition for CFS has undergone a number of revisions over the years. When different research groups use different definitions of the disease, it becomes difficult to compare findings. Most importantly, there is no indicator or diagnostic test that can be used to identify CFS, and since diagnosing CFS is a long and difficult process, cohorts established by different investigators vary, leading to different findings, confusion, and contention. In contrast, AIDS was readily identifiable and easily diagnosed once a blood test for HIV was developed.

Another problem is that in contrast to their excellent work on AIDS, the CDC has stumbled when tackling CFS. The CDC has dismissed evidence that CFS is an organic disease, and spent funds on investigating psychiatric and trauma-related causes, rather than infectious origins. The agency also diverted funds designated for CFS to other programs. These and other missteps alienated the CFS patient community—the opposite of what the agency accomplished with the AIDS community.

In part due to the standardized case definition of AIDS, identification of a candidate virus was relatively rapid. Determining its role in the disease was facilitated by the development of a blood test, which could be used to prove that HIV-1 caused AIDS. The relationship between HIV and AIDS was further confirmed by the development of antiviral drugs that inhibited viral replication and helped alleviate the symptoms of the disease.

Why have investigators failed to identify a virus behind CFS? (It is not due to the lack of appropriate technology; this has improved substantially since the 1980s with the development of polymerase chain reaction and rapid DNA sequencing.) One explanation for this dilemma is that an infectious agent does not cause CFS. However, there is plausible evidence for an infectious etiology, including observations that the disease is known to occur in outbreaks. Furthermore, in many cases the onset of symptoms appears to begin with a flu-like illness. Additionally, CFS is a heterogeneous disease, and may be caused by several different agents or a combination of viruses and non-infectious conditions. Another possibility is that an infection initiates an immune response that spirals out of control, leading to CFS symptoms. This scenario implies that at least some CFS patients have underlying deficits in immune regulation. If that’s true, it will be very difficult to identify the virus involved because it will likely have been eliminated from patients’ systems by the time CFS symptoms become apparent.

In retrospect, it is clear that the properties of AIDS made it an easy disease to understand. While the path to understanding CFS has been clouded by non-scientific issues, in the end the main reason why we do not understand this disease is because it is extraordinarily complex. But that never stopped a good scientist.

Thursday, January 5, 2012

Another xenotropic virus that can infect humans has been found by Dr Sandra Ruscetti in a Lung cancer cell line

Viruses 2011, 3(12), 2442-2461:

The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus

Joan L. Cmarik * , Jami A. Troxler, Charlotte A. Hanson, Xiang Zhang and Sandra K. Ruscetti

Laboratory of Cancer Prevention, National Cancer Institute-Frederick, Frederick, MD 21702, USA

* Author to whom correspondence should be addressed.

Received: 26 October 2011; in revised form: 22 November 2011 / Accepted: 9 December 2011 / Published: 19 December 2011

Download PDF Full-Text [619 KB, uploaded 19 December 2011 11:55 CET]

Abstract: The cell lines of the NCI-60 panel represent different cancer types and have been widely utilized for drug screening and molecular target identification. Screening these cell lines for envelope proteins or gene sequences related to xenotropic murine leukemia viruses (X-MLVs) revealed that one cell line, EKVX, was a candidate for production of an infectious gammaretrovirus. The presence of a retrovirus infectious to human cells was confirmed by the cell-free transmission of infection to the human prostate cancer cell line LNCaP. Amplification and sequencing of additional proviral sequences from EKVX confirmed a high degree of similarity to X-MLV. The cell line EKVX was established following passage of the original tumor cells through nude mice, providing a possible source of the X-MLV found in the EKVX cells.

Keywords: EKVX; NCI-60; human cell line; xenotropic murine leukemia virus; gammaretrovirus

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Cite This Article

MDPI and ACS Style

Cmarik, J.L.; Troxler, J.A.; Hanson, C.A.; Zhang, X.; Ruscetti, S.K. The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus. Viruses 2011, 3, 2442-2461.

AMA Style

Cmarik J.L., Troxler J.A., Hanson C.A., Zhang X., Ruscetti S.K. The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus. Viruses. 2011; 3(12):2442-2461.

Chicago/Turabian Style

Cmarik, Joan L.; Troxler, Jami A.; Hanson, Charlotte A.; Zhang, Xiang; Ruscetti, Sandra K. 2011. "The Human Lung Adenocarcinoma Cell Line EKVX Produces an Infectious Xenotropic Murine Leukemia Virus." Viruses 3, no. 12: 2442-2461.

Friday, December 30, 2011

Professor Simon Wessely once again attempts to defend the indefensible

Margaret Williams, meactionuk.org.uk:

Defending the indefensible?

Margaret Williams 27^th December 2011

Professor Simon Wessely once again attempts to defend what has already been shown to be indefensible, namely his own beliefs about the nature of ME/CFS, including his belief that graded exercise therapy (GET) has “an impeccable safety record” (Simon Wessely; Health in mind and body; The Journal of the Foundation for Science and Technology: 2011:20:7: 9 –11).

The article contains so many insupportable assertions that it cannot go unchallenged.

In his article, although he does not mention ME as such, Wessely refers to Chronic Fatigue Syndrome (CFS), but in countless articles published in medical journals, reports from official bodies such as the Joint Royal Colleges, in medical textbooks and in the media, as well as in the PACE Trial literature itself, the Wessely School insist that ME and CFS are synonymous.

In this latest article (the publishing of which is perhaps surprising, given his frequent assertions that he has relinquished his work on ME/CFS and that he no longer feels safe publishing about the disorder because of the death threats he has received, and that he now feels safer in Afghanistan), Wessely conforms to his track record of appearing to form his conclusions before he has generated the data to support his conclusions (he often states his assumptions and beliefs as though they are established fact, for example, he has asserted that people with ME benefit from “adopting the sick role” and from “secondary gain”, and that what “precipitates” ME is not what “perpetuates” it, all of which are supposition not supported by data; a further illustration is to be seen in his study of Vitamin B status in just 12 CFS patients in which he found evidence of reduced functional vitamin B status but concluded: “clearly, many patients with CFS are currently taking vitamin B…with little evidence of benefit”, yet nowhere does he provide any evidence that “many” patients are taking supplements with little evidence of benefit and his final conclusion again fails to follow from his data: JRSM 1999:92:183-185).

Wessely’s assertions in his current article are of particular interest because they provide such clear illustration of his cognitive biases, for example:

“CFS illustrates the gap that lies between physical health/illness on the one hand and mental health/illness on the other”: all life-destroying diseases affect both physical and mental health, not just ME/CFS.

“CFS is a multi-factorial illness”: Wessely does not know this, since the cause remains unknown.

“To understand why some people do not get better as the months and years go by, one has to look at behavioural and psychological factors”: this is nothing more than Wessely’s assumption; people do not recover from multiple sclerosis or from motor neurone disease, so it is telling that he makes an exception only in the case of one particular classified neurological disorder (ME/CFS): why do so, unless it is as a face-saving measure because for the last 25 years the Wessely School have rigidly and unscientifically conflated psychiatric fatigue with ME/CFS?

“The illness is then a complicated mixture of predisposition, precipitation, and perpetuation”: Wessely states this as though it were proven fact, but it is unproven and his inability to recognise this demonstrates a fundamental misunderstanding of the nature of scientific knowledge.

“A landmark trial on the management of CFS, known as the PACE Trial, was published recently in The Lancet….Two treatments, graded exercise and CBT, clearly made a difference, although they were certainly not ‘magic bullets’: not only were the interventions used in the PACE Trial very far from being magic bullets, the Chief Principal Investigator himself described them as being “only moderately effective”.

“For those who appreciate these things, the trial is a thing of beauty”: for those who appreciate these things, the PACE Trial -- which cost £5 million -- has been described as a travesty of science and a tragedy for patients; the conclusions were flawed; the primary outcome measures were dropped; ratings that would qualify a participant as sufficiently impaired to enter the trial were deemed by the Principal Investigators (PIs) to be “within the normal range” when recorded on completion of the trial; there were significant conflicts of interest in that all three PIs work for the insurance industry (whose managers insist that claimants undertake a course of CBT and GET -- called “rehabilitation” -- which, if people are too ill to do so or if they know from their own experience that it makes worse and therefore decline, payments are stopped on the basis that claimants do not to want to get better); the PIs intentionally studied a heterogeneous population and it was conceded only after publication of the results in The Lancet that the Investigators did not purport to be studying ME; there was a failure to control the trial; there was downgrading of what constituted serious adverse events; there were many changes to the entry criteria; data was not reported and objective outcome measures were dropped; methods of scoring were changed so as to produce minimally better results, and the results were blatantly misreported in The Lancet (see http://www.meactionuk.org.uk/COMPLAINT-to-Lancet-re-PACE.htm and see also http://www.meactionuk.org.uk/Normal-fatigue.htm ).

“We now have two treatments that we can recommend with confidence to our patients. However, the story does not quite end there. Patient groups rejected the trial out of hand, and the internet was abuzz with abuse and allegations. The main reason for this depressing reaction was the stigma that attaches to disorders perceived (rightly or wrongly) to be psychiatric in origin”: the reason people with ME/CFS reject CBT and GET is because they do not work, but Wessely refuses to accept this, so he here provides an explanation already shown by his own research to be incorrect.

He has previously written: “CFS sufferers are also usually portrayed as hostile to psychological explanation, mental illness, and psychiatry in general….This study aims to investigate attitudes of CFS patients to psychiatric illness (and) a comparison group of patients with rheumatoid arthritis (RA) was chosen….We began with the following hypotheses: CFS patients have more negative attitudes to mental illness…(represented by the perceived stigma of psychiatric illness)…(and) failure to identify emotional states (alexithymia) contributes to denial of the role of psychiatric disorders in the aetiology of CFS….Contrary to our hypotheses and the media accounts of CFS, we found no evidence that CFS patients are characterized by particularly hostile attitudes to mental distress….Our study also failed to demonstrate any overall differences in personality traits that may underlie negative attitudes to mental illness or psychiatry….The… alexithymia scores found in the CFS compared with the RA patients were contrary to our original hypothesis….There was no difference between CFS and RA patients in hostility to mental illness….This study provides no evidence to support the anti-psychiatry tone that is so striking in the popular literature on CFS” (Personality and Social Attitudes in Chronic Fatigue Syndrome. Barbara Wood and Simon Wessely; J Psychsom Res 1999:47:4:385-397).

“If one obtained identical results to the PACE trial, but this time with anti-viral drugs, the reaction would have been totally different. This is exactly what did happen when a very small trial of a drug that modulates the immune system (and which has some nasty side effects) was greeted with acclaim from the same sources that tried to discredit the PACE trial, which tested interventions with an impeccable safety record”: GET for people with ME does not have an impeccable safety record. Indeed, there is abundant evidence from numerous surveys by ME/CFS charities of almost 5,000 patients that in such patients CBT is ineffective and that GET is unacceptable and sometimes positively harmful.

Those surveys include one sponsored jointly by the ME Association and Action for ME (“Report on a Survey of Members of Local ME Groups”. Dr Lesley Cooper, 2000). Cooper found that “Graded exercise was felt to be the treatment that made more people worse than any other” and that it had actually harmed patients

(http://www.afme.org.uk/res/img/resources/Group%20Survey%20Lesley%20Cooper.pdf).

Another survey of 2,338 ME/CFS sufferers (“Severely Neglected: M.E. in the UK”) was carried out in 2001 by Action for ME; its preliminary report stated: “Graded exercise was reported to be the treatment that had made most people worse”; in the final report, this was changed to stating that graded exercise had made 50% of patients worse

(http://www.afme.org.uk/res/img/resources/Severely%20Neglected.pdf).

The 25% ME Group for the Severely Affected carried out a further survey in 2004 which found that 93% of respondents found GET to be unhelpful, with 82% reporting that their condition was made worse (http://www.25megroup.org/Group%20Leaflets/Group%20reports/March%202004%20Severe%20ME%20Analysis%20Report.doc).

In 2005, a report (“Our Needs, Our Lives”) published by The Young ME Sufferers Trust found that 88% had been made worse by exercise (http://www.tymestrust.org/pdfs/ourneedsourlives.pdf).

In June 2007, through Section 16b funding from the Scottish Government, Action for ME produced a report “Scotland ME/CFS Scoping Exercise Report”, which found that 74.42% were made worse by GET.

In 2008, Action for ME published another survey of over 2,760 patients (“M.E. 2008: What progress?”) which found that one third had been made worse by GET and that at their worst, 88% were bed/housebound, being unable to shower, bathe or wash themselves, and that 15% were unable to eat unaided. The Press Release of 12^th May was unambiguous: “Survey finds recommended treatment makes one in three people worse” (http://www.afme.org.uk/news.asp?newsid=355).

In 2009, the Norfolk and Suffolk ME Patient Survey of 225 respondents stated: “Respondents found the least helpful and most harmful interventions were Graded Exercise Therapy and Cognitive Behavioural Therapy” (http://www.norfolkandsuffolk.me.uk/surveylink.html ).

The International Association of CFS/ME recently published an article by Tom Kindlon (Bulletin of the IACFS/ME: 2011:19(2):59-111: Reporting Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) that details the high rates of adverse reactions to exercise, as well as dissecting the PACE Trial in relation to the heterogeneity of subjects, the tracking of adverse events and the lack of objective outcome measures.

As Ed Lewisohn correctly points out in correspondence relating to the Frenchay Hospital’s clinic at Bristol: “You refer to ‘Frenchay Hospital’s specialist chronic fatigue, or ME clinic’, but ME is an incurable neurological condition and cannot be synonymous with chronic fatigue. Chronic fatigue syndrome is treated by psychiatrists with graded exercise therapy, but if exercise makes (it) better, then that condition is not ME….But many patients with ME are also sent to chronic fatigue centres and receive the same treatment: they are then, shockingly, made more ill” (http://www.thisisbristol.co.uk/chronic-fatigue-syndrome/story-14243686-detail/story.html ).

There is thus an abundance of empirical evidence that GET can result in high rates of adverse effects.

Why is it that the Wessely School, who claim to be so committed to evidence-based medicine (EBM), are permitted to continue to disregard the evidence that proves them to be wrong about the nature of ME and about the efficacy of GET in those suffering from it?

The answer may be because, like so many of the Wessely School myths, EBM does not actually exist.

In 2009 Bruce Charlton, Professor of Theoretical Medicine at the University of Birmingham, clarified the facts in relation to EBM: “It is obvious that EBM was from its very inception a Zombie science….A Zombie science does not perform any scientific function, so it is invulnerable to scientific critique since it is sustained purely by the continuous pumping of funds….The massive success of EBM is that it has rationalised the takeover of UK clinical medicine by politicians and managers….Zombie science is not driven by the scientific search for truth (and it is) kept moving for so long as it serves the purpose of its funders….EBM embraced a top-down and coercive power structure to impose EBM-defined ‘best evidence’ on clinical practice, whether clinical scientists or doctors agreed that the evidence was best or not….Expertise was arbitrarily redefined (and) virtue redefined as submission to EBM recommendations, so the job of physician was at a stroke transformed into one based upon absolute obedience to the instructions of EBM-utilising managers. Indeed, since too many UK doctors were found to be disobedient to their managers, in the NHS this has led to a progressive long-term strategy of the replacing doctors by more-controllable nurses, who are now the first contact for patients in many primary and specialist health service situations…. EBM was not a real science, indeed, it wasn’t any kind of science at all (and) it was not adopted by scientists but by politicians, government officials, managers, and biostatisticians….When the UK government understood that what was being proposed was a perfect rationale for re-moulding medicine into exactly the shape they had always wanted it, the NHS hierarchy were falling over each other in their haste to establish this new orthodoxy in management, medical education and in founding new government institutions such as NICE….Suddenly, the Zombie science of EBM was everywhere in the UK…unhampered by inconveniences such as truthfulness or integrity…it was being practised by many individuals…who lacked…any training and experience in clinical medicine and who certainly did not provide direct patient care….Here was a doctrine which advocated rejecting and replacing with itself the whole model of medical science and practice of the past. It advocated a new model of health service provision, new principles for research funding, a new basis for medical education. And the evidence for this? Well, none. Not one particle. ‘Evidence-based’ medicine was based on zero evidence (but it) was proclaimed Messiah with the backing of serious amounts of UK state funding…to create a fairly-realsitic Zombie of pseudo-science….Nowadays, EBM means whatever the political and managerial hierarchy of the health service want it to mean for the purpose in hand” (Zombie science of Evidence-Based Medicine. Bruce G Charlton. Journal of Evaluation in Clinical Practice 2009:15:930-934).

EBM, however, has proved invaluable to the Wessely School in the perpetuation of their own myths about and management of ME/CFS, to the advantage of both the state and the insurance industry.

Despite the relentless determination of the Wessely School to claim ME/CFS as a functional somatoform disorder (in his latest article, Wessely reiterates his claim that: “the greater the number of symptoms, the more likely the patient was to develop a mood or anxiety disorder”), medical science is at last ensuring that the Wessely era is coming to an end.

Whilst XMRV is now thought to be a laboratory contaminant (and the triumphant glee of those who rejoiced at this is to be greatly deplored), the role of a retrovirus has not yet been resolved: indeed, Dr Ian Lipkin of Columbia University and chief virus-hunter for the NIH was reported on the Wall Street Journal blog on 27^th December 2011 by Amy Dockser Marcus to have said that all the scientists and doctors involved in the NIH study, including the authors of the retracted PNAS and Science papers, “are committed to completing this study because none of us believes that the issue of retroviral infection in CFS/ME is resolved”.

Retrovirology apart, there is now undeniable evidence of multi-system damage in ME/CFS, including inflammation of the blood vessels, hypoperfusion of the brain, delayed recovery of muscles after exercise, dysfunction of the immune and neuroendocrine systems, and evidence of marked abnormalities in gene expression profiling.

Professor Nancy Klimas is to head a new Institute for Neuroimmune Medicine (specifically ME/CFS) at Nova Southeastern University: she will be providing cutting edge research and education of health care professionals, combined with care of patients; she will focus on systems biology, connecting neuro-imaging experts with scientists researching inflammation and genomics/proteomics, as well as collaborating with experts in neurotoxicology.

There is also the work of Dr Jose Montoya’s Chronic Illness Initiative at Stanford; the husband and wife team of Drs Light at the University of Utah; Dr Derek Enlander’s Chronic Fatigue Initiative with a very large budget for research at Mount Sinai, as well as the Public Health and Neuroimmunology Unit (PHANU) at Bond University in Australia (http://forums.phoenixrising.me/content.php?519), plus the committed work of Professors Mark VanNess and Christopher Snell at the University of the Pacific, all of which disprove the beliefs of the Wessely School that ME/CFS is a behavioural disorder.

Furthermore, the UK Medical Research Council has finally recognised the need for biomedical research into ME/CFS and is funding £1.6 million for research into aspects including autonomic dysfunction, aberrant mitochrondrial and cytokine production in skeletal muscles, and immune system dysfunction.

As clinical psychologist Dr Dorothy Rowe pointed out in 1993: “People who know absolutely that they are right are very dangerous” (The Observer, 14^th November 1993), but who paid any attention? Father Cormac Rigby did: “The greatest enemies of truth are those who think they have a monopoly of truth” (The Lord be with you; Family Publications, Oxford, 2004).