Research hypothesis | post-XMRV, could there still be an overlapping infectious agent? | 1 December 2012

December 1, 2012

From Muscular Disorders, 1 December 2012.

Uvo Rovigatti
Department of Oncology, Transplantation and New Biomedical Technologies, University of Pisa Medical School, Pisa, Italy

Chronic Fatigue Syndrome (CFS) and Cancer Related Fatigue (CRF): two “fatigue” syndromes with overlapping symptoms and possibly related aetiologies


In July 2010, at the Muscle Fatigue Meeting, I presented an overview of Chronic Fatigue Syndrome and Cancer Related Fatigue, emphasizing a critical interpretation of the potential association between Chronic Fatigue Syndrome and Cancer Related Fatigue and a newly discovered retrovirus: Xenotropic Murine Related Virus.

Since this association was hotly debated at that time, I suggested at the Meeting that it was wrong and most likely due to the identification of the wrong virus culprit. Today, 20 months after the Meeting, the first part of our prediction has turned out to be correct, as Xenotropic Murine Related Virus was shown to be a laboratory-created artefact.

Still, the potential association of fatigue-syndromes with an infection (most likely viral) is sustained by a plethora of evidence and this overview will initially summarize data suggesting prior viral infection(s). The principal hypothesized mechanisms for both peripheral and central Chronic Fatigue Syndrome/Cancer Related Fatigue will be then summarized, also indicating plausible associations and triggering factors.

All evidence accrued so far suggests that further research work should be performed in this interesting area and in order to identify an infectious agent for Chronic Fatigue Syndrome/Cancer Related Fatigue. One candidate RNA virus, Micro-Foci inducing Virus, will be described in this overview.

MEA note: Our medical adviser, Dr Charles Shepherd, writes: “I know that some people do not agree but this paper supports the view taken by both the MEA and the MRC Expert Group that studies involving people with other illnesses that have either significant central (brain) fatigue or peripheral (muscle) fatigue have to form PART of our research portfolio because there may well be overlapping mechanisms involved.

4 thoughts on “Research hypothesis | post-XMRV, could there still be an overlapping infectious agent? | 1 December 2012”

  1. Fatigue is a word with an incredible number of meanings from weakness to exhaustion. Many people with ME also do not report that they have this and it was never included in Ramsay’s original description of ME. No other neurological disease is defined or given a name after a common symptom.

    There is simply no reason at all to use money to study other diseases, unless people think either ME shouldn’t be funded or they would rather the money go to different diseases, both of which would be disgraceful.

    Scientists know that it is impossible to study ME by looking at other diseases. No one else would expect this to happen with their disease so why should ME patients?

    Why does the MEA think it is acceptable, when there is little research on ME and virtually no ME scientific research, to therefore agree with taking that money and putting it into different diseases? Or is this only the view of Charles Shepherd who is after all not a scientist?

    The MRC group who are focussed on fatigue, many of whom are also not ME scientists, are also not looking at ME but fatigue. Which is proven by their comments on the disease they are funding, using of what was claimed to be ME money.

    As an important side issue, what retorviruses have been detected by Dr Mikovits with unbiased methods is still to be explored. This data obtained with NGS and serology is not in doubt.

  2. While I know there is woefully inadequate funding for biomedical research into ME (and everything should be done to improve this dire situation) we should not discount the possibility of insights and treatments that may benefit ME sufferers through the research into other diseases with overlapping/similar symptoms. In the past when research has been conducted into a particular illness, it has sometimes led to a ‘breakthrough’ in the understanding and treatment of another illness e.g. I was very interested in the recent TGI Friday weekly round-up of research updates concerning the drug Dilmapimod for nerve pain, whilst not being a study/trial for nerve pain in ME, it may have possible benefits for those who suffer distressing nerve pain as part of their ME especially with its mechanism of working on the immune system. Also, the Norwegian study using an anti-cancer drug in the possible treatment of ME could lead to better understanding for future researchers.
    As a long-term severe ME sufferer I feel we should be open to biomedical scientific research that could shed some light and some possibility of relief through treatments for this devastating illness with all its distressing symptoms. I for one welcome any step forward that takes ME away from the useless CBT/GET.

    1. It is impossible to research ME by studying people with a different disease. This will not bring insights about ME. It is as bad as studying the CFS/ME or encephalopathy.

      The example you give (Dilmapimod) has not been tested on ME patients, so it is impossible to know if this should be used for ME or is an effective treatment for ME. However the Norwegian study may have contained ME patients, but this cannot be claimed as the definition used was not an ME definition and used no objective tests for diagnosis.

      Having funding taken away from ME research has nothing to do with being open. If ME patients were to get all funding from the MRC next year will others with different diseases be told they are not being open to the possibility of what ME could tell them about their disease? No, they would not expect to be treated this way and ME patients shouldn’t either.

  3. Many people who develop CFS/ME originaly developed glandular fever. Dr Shepherd claims his illness was as a result of chicken pox. Both glandular fever and chicken pox are mild illnesses in young children when they were normally esperienced until recent times.This raises the question as to whether the juvenile immune system is designed to handle childhood viral infections in the way that the adult (or adolescent) immune system is not, possibly because of the shrinking of the thymus, either because the immune system overreacts, or is unable to prevent permanent organ damage, or does not shut down after the acute illness. It is noteworthy that females are more prone, but are they more prone to serious outcomes if the same infections are experienced in childhood, or is the adult (or adolescent) female immune system, designed to protect a foetus, less able to tackle the infection than that of the male?

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