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 (

In a specially commissioned piece for the charity Invest in ME, the researchers say:

Dr John Chia, an infectious diseases specialist from Torrance, California, who specialises in ME/CFS, is on record: The CFIDS Chronicle (Research Update, Summer 1993) explained viruses and retroviruses as follows:

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 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:

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

De Freitas was publicly discredited; her research funding was discontinued and her research abandoned; she was subjected to what appeared to be attempts to destroy her professional reputation. Commenting on the subsequent discovery of XMRV (see below), ME/CFS expert Dr Paul Cheney of The Cheney Clinic was unambiguous: In August 1991, together with co-author Brendan Hilliard, Elaine De Freitas had applied for a world patent that was subsequently issued in April 1992. Detailed information has been provided by Dr Alan Cocchetto, Medical Director of The National CFIDS Association [National CFIDS Foundation] ( ). Cocchetto is clear: It has been said that De Freitas’s reputation was intentionally destroyed because her research did not support the theory that (ME)CFS is a psychoneurosis, and that her public discrediting caused others to fear following up her work (Co-Cure;NOT: 16th October 2009). As Neenyah Ostrom commented: There undoubtedly seems to be collaboration about policy concerning ME/CFS between the UK Wessely School and Dr William (Bill) Reeves, Principal Investigator of the CDC’s CFS research programme, who is held in the same disregard in the US as Professor Simon Wessely is held in the UK (see below). Regarding blood donation by people with ME/CFS, it is a matter of record that in reply to a letter dated 21st December 1991 from the late Joan Irvine, on 16th January 1992 Dr George Rutherford, Chief of the Infectious Diseases Branch of the US Department of Health and Human Services, replied to her query about blood donation by people with (ME)CFS:

Also on 16th January 1992, the same Dr William Reeves of the CDC wrote to Joan Irvine about the same issue:

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 ( ). The Project Number is 1R01A1078234-01A2 and the description provided by the applicants says:

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,

In contrast, in their article in Science Mikovits et al deal with science, not speculation:

Last Update 19/11/2011