A New Decade of ME Research: The 11th Invest in ME International ME Conference 2016
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Stealth Adapted Viruses

Discussion in 'General ME/CFS Discussion' started by w john martin, Apr 30, 2014.

  1. w john martin

    w john martin

    Dear Members,

    I am pleased to inform you of a renewed effort to focus attention on stealth adapted viruses as the cause of CFS. I did so by submitting the following public comment to the Institute’s of Medicine Committee for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome:

    Dear Sir,

    Members of the Committee on Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome could benefit by learning about stealth adapted viruses. These viruses lack the relatively few virus coded components normally targeted by the cellular immune system. The brain is particularly susceptible to symptomatic illness caused by stealth adapted viruses. Based on extensive virus culture studies, these illnesses include the chronic fatigue syndrome (1).

    Government sponsored reluctance in accepting the existence of stealth adapted viruses is mainly because of the unequivocal origin of some of these viruses from the kidneys of monkeys used to generate polio virus vaccines (2).

    Fortunately, the body has an effective non-immunological defense mechanism mediated by the alternative cellular energy (ACE) pathway. This pathway can suppress both stealth adapted and conventional viruses and can be easily enhanced through the consumption of enerceutical foods and activated liquids and by other methods.

    It is time for an international effort to redefine a major category of illnesses with impaired brain functioning as stealth adapted virus encephalopathy. Efforts to overly sub-classify this heterogeneous grouping of illnesses are far less important than moving forward with effective prevention and treatment strategies. The Institute of Medicine committee members could help in these efforts by learning more about stealth adapted viruses and the ACE pathway and by openly discussing and resolving the politically sensitive issues with senior public health officials.

    1. Martin WJ et al. Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with chronic fatigue syndrome. Am. J. Pathol. 145: 440-451, 1994. (Available online via PubMed).

    2. Martin WJ et al. African green monkey origin of the atypical ‘stealth virus’ isolated from a patient with chronic fatigue syndrome. Clin. Diag. Virol. 4: 93-103, 1995.


    W. John Martin, MD, PhD.
    Last edited by a moderator: Jun 27, 2014
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  2. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia
    I was interested in this research a few years after it was first published. I was at the conference where you gave this talk:


    I neither believe nor disbelieve in the importance of this kind of virus in ME or CFS. What I think though is that there is sufficient evidence that other researchers should have been interested, and serious consideration should have been given to funding this research in any grant proposal. Things like this should not be left to hang in the scientific record, we need definitive answers.

    The problem for the IOM, like with other areas in ME/CFS research, is a lack of independent replication, and sufficient studies to demonstrate its diagnostic or causal. In particular we need studies showing diagnostic specificity and sensitivity. Evidence based medicine is about translation from science to clinical practice in a managerial setting, using managerial criteria. Its not science, its about managing science with an eye toward clinical use. There is a barrier to research being properly considered.
    Last edited: Apr 30, 2014
    SOC likes this.
  3. PNR2008

    PNR2008 Senior Member

    OH USA
    I tested positive for stealth virus when I went to Jay Goldstein MD in about 1993.
    beaker likes this.
  4. heapsreal

    heapsreal iherb 10% discount code OPA989,

    australia (brisbane)
    Please keep us updated John.
    I believe my issues are cmv related and have had some good results with antivirals. The stealth virus theories were some of the first info i found online relating cmv with cfs/me.

  5. ukxmrv

    ukxmrv Senior Member

    It's great to see you posting to CFS groups after so long Dr Martin. Thank you.
    beaker and heapsreal like this.
  6. anciendaze

    anciendaze Senior Member

    While I remain agnostic w.r.t. specific pathogens, I am firmly of the belief that there are multiple paths by which a virus can achieve stealth. We have been through multiple flaps concerning retroviruses, which can insert provirus which then remains in cells for life. We have recently seen that even a well-known herpes virus like EBV may be able to replicate DNA without killing host cells. This opens the possibility that it can exploit clonal expansion of host immune cells. We already know that VZV, another herpes virus, can persist in the CNS for most of a lifetime.

    Both types of virus capable of stealth, retroviruses and DNA viruses, depend on defects in host immune response needed to avoid autoimmune action against host cells containing DNA from HERVs. This limits immune activity against both retroviruses and DNA viruses, which some have clearly managed to exploit. I doubt the list is complete.

    In this context, I think the discovery last year of a large number of copies of HERV-K111 which had previously been overlooked, and were not found in genomes of prehistoric humans, points toward a particularly active region of human genomes. Only one copy has turned up in chimpanzees, half a dozen in prehistoric humans, and more than 100 in modern humans. It also seems that all modern humans cannot be assumed to have the same HERVs in the same places. This is strong evidence of recent or current activity.

    I think it is very significant that the big expansion in activity appears to have coincided with the change in the number of humans living together in a group. Pathogens specifically adapted to humans must have become more prevalent as the environment in which humans lived became dominated by other humans. This has ominous implications for a world in which seven billion humans are all part of a single rapidly-connected population. We respond pretty well to something as obvious as Ebola, but diseases with longer latency can penetrate far into a susceptible population before we notice. If the diseases caused are not entirely new, we may not notice at all.

    Three genes which have turned out to be intimately involved in detection of and defense against nucleic acids from retroviruses are: APOBEC3, TRIM5alpha, SAMHD1. There are already studies showing correlations between SNPs in these genes and specific diseases with currently unknown etiology. This is a strong indication that viral pathogens and defenses against them are specifically involved. To me it looks like many lines of research are converging on viruses and viral defenses.

    We have also seen one study specifically indicating activation of microglia in ME/CFS.

    At this point I have no doubt we are looking at infectious agents which evade many means of detection, or the response to these, but the likelihood of immune defects makes me suspect these will not be unique.

    It is not enough to simply say that a pathogen implicated in a disease does not behave like those you prefer to work with, or that the disease is the result of the response rather than the pathogen itself. These are all ways of declaring the disease "somebody else's problem". Nature does not notice academic distinctions.

    Degenerative neurological diseases and cancers are also showing up in connection with very similar highly-specific patterns of gene activation and immune responses, or defects in immune response. If a narrow, highly-localized failure of immune response is responsible, it may never be possible to identify a "cause" in the sense that many researchers have been trying to explain these diseases. The "causes" may be normal random variations in internal milieu, and the real problem may be a failure to repair defects or respond appropriately to challenges. Most methods of detection used in the past would not show such specific and localized immune defects.

    With those who live long enough facing about one chance in three of dementia, and a substantial risk of incapacitation due to Parkinson's disease, and cancer considered the second greatest cause of death, we are no longer talking about minor medical mysteries which can be allowed to persist while turf wars take place between researchers.
    NK17, cigana and PNR2008 like this.
  7. beaker

    beaker ME/cfs 1986

    I tests positive too, only via Cheney sending it to Martin.
    PNR2008 likes this.

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