MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
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194<br />
(said) ‘Whatever causes CFS, it isn’t the virus itself’…Anthony Clare, psychiatrist and medical director of St<br />
Patrick’s Hospital <strong>in</strong> Dubl<strong>in</strong> (now deceased), po<strong>in</strong>ted out that…there have been many ‘fatigue’ diseases with shift<strong>in</strong>g<br />
causes: ’Neurasthenia, food allergies, now viruses. Some people would always rather have a disease that might kill<br />
them than a syndrome they have to live with’ ” (Science 1990:249:4974:1240).<br />
In their PNAS article that was published <strong>in</strong> April 1991, De Freitas et al noted that chronic fatigue immune<br />
dysfunction syndrome (CFIDS) “may be related or identical to myalgic encephalomyelitis” and exam<strong>in</strong>ed adult<br />
and paediatric CFIDS patients for evidence of human retroviruses (HTLV types I and II). As the CFIDS<br />
Chronicle article noted, the Wistar team looked at the peripheral blood DNA to see if they could f<strong>in</strong>d<br />
messenger RNA (mRNA) encod<strong>in</strong>g for a viral segment of the HTLV‐II virus.<br />
At that time, known human retroviruses were the human immunodeficiency viruses 1 and 2 (HIV‐1 and<br />
HIV‐2) which are known to cause AIDS, and human T‐lymphotropic viruses HTLV‐I which causes<br />
lymphoma and HTLV‐II which causes leukaemia (Hunter‐Hopk<strong>in</strong>s <strong>ME</strong>‐Letter, October 2009). The four<br />
segments of the HTLV‐II virus are referred to as the env, gag, pol and tax.<br />
After a two‐year study, De Freitas et al provided evidence for HTLV‐II‐like <strong>in</strong>fection of blood cells from<br />
CFIDS patients (and also to a lesser extent from people closely associated with them). This evidence was<br />
further substantiated by patient reactivity to prote<strong>in</strong>s with the molecular weights reported for HTLV‐I and<br />
HTLV‐II antigens.<br />
In their article, De Freitas et al said: “The frequency of these antibodies <strong>in</strong> CFIDS patients compared with healthy<br />
non‐contact controls suggests exposure / <strong>in</strong>fection with an HTLV‐like agent rare <strong>in</strong> healthy non‐contact people”.<br />
Whilst none of the CFIDS patients’ blood samples conta<strong>in</strong>ed detectable HTLV‐I gag sequences, DNA from at<br />
least two separate bleed<strong>in</strong>gs was positive for the HTLV‐II gag subregion <strong>in</strong> 83% of adult and 72% of<br />
paediatric CFIDS patients, and the authors po<strong>in</strong>ted out that “similar frequencies of PBMCs (peripheral blood<br />
mononuclear cells) express<strong>in</strong>g retroviral mRNA have been reported for HIV‐<strong>in</strong>fected <strong>in</strong>dividuals…The cl<strong>in</strong>ical<br />
histories of these CFIDS patients do not reveal behavioural or genetic factors usually associated with retroviral<br />
<strong>in</strong>fection. Yet our data suggest that not only are these HTLV‐II‐like genes and HTLV‐reactive antibodies associated<br />
with CFIDS <strong>in</strong> patients but that samples from a significant proportion of their non‐sexual contacts are positive”.<br />
De Freitas et al were careful to emphasise that “Although our data support an association between an HTLV‐like<br />
agent and CFIDS, we cannot, as yet, def<strong>in</strong>e the agent’s role <strong>in</strong> the disease process. It may be a secondary <strong>in</strong>fection to<br />
which immunologically compromised patients are susceptible. Alternatively, it may be one of two viruses that, when<br />
co‐<strong>in</strong>fect<strong>in</strong>g the same haematopoetic cells, <strong>in</strong>duce immune dysfunction”.<br />
Follow<strong>in</strong>g the Wistar f<strong>in</strong>d<strong>in</strong>gs, researchers at the US Centres for Disease Control (CDC) allegedly attempted<br />
to replicate De Freitas’ work but failed to do so; this was suggested to be because certa<strong>in</strong> scientists appeared<br />
eager to discount any possibility of a retroviral association with CFIDS. De Freitas defended her work and<br />
<strong>in</strong>sisted that the CDC <strong>in</strong>vestigators had modified her assays, with the result that her work could not be<br />
replicated by the CDC. It is known that attempts to replicate De Freitas’ work differed substantially from<br />
her own work <strong>in</strong> a number of ways, <strong>in</strong>clud<strong>in</strong>g the cl<strong>in</strong>ical def<strong>in</strong>ition of patients studied; uniform failure to<br />
use a “hot start” procedure with the PCR assay to maximise the efficiency of the PCR reaction, and the use<br />
of experimental conditions for the PCR assay that differed significantly from those used by De Freitas et al<br />
(Co‐Cure RES: 6 th March 2002).<br />
De Freitas was publicly discredited; her research fund<strong>in</strong>g was discont<strong>in</strong>ued and her research abandoned;<br />
she was subjected to what appeared to be attempts to destroy her professional reputation. Comment<strong>in</strong>g on<br />
the subsequent discovery of XMRV (see below), <strong>ME</strong>/CFS expert Dr Paul Cheney of The Cheney Cl<strong>in</strong>ic was<br />
unambiguous: “Her work was unfortunately assaulted by the CDC. Her proposal to fly to the CDC <strong>in</strong> Atlanta to<br />
physically run the assays side by side with the CDC scientists was dismissed by the CDC”<br />
(http://cheneycl<strong>in</strong>ic.com/a‐retrovirus‐called‐xmrv‐is‐l<strong>in</strong>ked‐to‐cfs/538 ).