Monday, September 20, 2010


From a 1995 article by Dr. Dharam Ablashi:  "At the CFS Research and Clinical Conference 1994, Diack et. al. reported the identification of retrovirus particles from the peripheral blood lymphocytes of 10/34 CPS patients and none of the controls. The majority of viral particles were similar to the ultra structure of visna virus (lentivirus) and murine leukemia virus. According to the authors, virus-like structures were compatible with various maturation stages of lentivirus. No reverse transcription activity or possible target cell phenotype was found. Considerable work is needed to prove that these ultra-structures resembling a retrovirus are not artifacts."

Diack D, Easingwood R, Cross J, Carlisle B, et. al. Electron microscopic immunocytologic profiles in Chronic Fatigue Syndrome. Proc Res & Clin CFS Conf. p. 24, 1994 (Oct. 7-11, Ft. Lauderdale, FL). 


  1. This is really interesting. Here it is mentioning viral particles that were similar to the ultra structure of visna virus (lentivirus), and the virus Elaine DeFreitas found has been characterized by some as a lentivirus, and murine leukemia virus, indicating that these researchers found them together. Since XMRV is a recombinant retrovirus, is it possible that what Elaine DeFreitas saw and photographed were viral particles in the process of becoming XMRV?

    Patricia Carter

  2. Thank you for digging up this history!

    Any chance you could set up an in-depth interview with Dr Byron Hyde? I know that he does not agree with the XMRV-as-solution approach. It would be informative to learn more about why not, and what direction he thinks research should be going in.

  3. The XMRV/MLV findings were exciting not from the standpoint of etiology or cause of CFS/ME but reversing the widely held belief that this was an imagined disease.
    It has not been shown that the virus or virions cause CFS/ME. Dr DeFrietas twenty years ago determined a retrovirus relationship. Attempts to treat this virus were unsuccessful. Retrovirus treatment has improved in the past two decades, so maybe new research maybe productive. Such research should begin with in Vitro lab work, killing the virus in lab tests.
    However caution should be exercised, the virus or virions may be superimposed and could proliferate due to immune dysfunction. This dysfunction being caused by other factors.

    Derek Enlander MD
    New York

  4. It is maddening to see that there were clear-cut, scientifically-derived clues to retroviral infection or implication in this illness, and these clues were ignored in favor of subjective, psychosomatic "explanations" and overly-inclusive, poorly defined cohort definition. Thank you for your work, Mindy.

  5. Hearty thanks, Dr. Endlander, for posting here!

  6. Dr. Enlander, you said: "Attempts to treat this virus were unsuccessful." Can you be more specific? Who attempted to treat DeFreitas' retrovirus? What were the results? Were any studies done? Published?

    Patricia Carter

  7. Attempts have already been made to kill the XMRV virus in Vitro. 5 drugs are effective.


    BACKGROUND: XMRV (xenotropic murine leukemia virus-related virus) is the first known example of an exogenous gammaretrovirus that can infect humans. A limited number of reports suggest that XMRV is intrinsically resistant to many of the antiretroviral drugs used to treat HIV-1 infection, but is sensitive to a small subset of these inhibitors. In the present study, we used a novel marker transfer assay to directly compare the antiviral drug sensitivities of XMRV and HIV-1 under identical conditions in the same host cell type.

    RESULTS: We extend the findings of previous studies by showing that, in addition to AZT and tenofovir, XMRV and HIV-1 are equally sensitive to AZddA (3'-azido-2',3'-dideoxyadenosine), AZddG (3'-azido-2',3'-dideoxyguanosine) and adefovir. These results indicate that specific 3'-azido or acyclic nucleoside analog inhibitors of HIV-1 reverse transcriptase (RT) also block XMRV infection with comparable efficacy in vitro. Our data confirm that XMRV is highly resistant to the non-nucleoside RT inhibitors nevirapine and efavirenz and to inhibitors of HIV-1 protease. In addition, we show that the integrase inhibitors raltegravir and elvitegravir are active against XMRV, with EC50 values in the nanomolar range.

    CONCLUSIONS: Our analysis demonstrates that XMRV exhibits a distinct pattern of nucleoside analog susceptibility that correlates with the structure of the pseudosugar moiety and that XMRV is sensitive to a broader range of antiretroviral drugs than has previously been reported. We suggest that the divergent drug sensitivity profiles of XMRV and HIV-1 are partially explained by specific amino acid differences in their respective protease, RT and integrase sequences. Our data provide a basis for choosing specific antiretroviral drugs for clinical studies in XMRV-infected patients. ''


    Susceptibility of the human retrovirus XMRV to antiretroviral inhibitors. Smith RA, Gottlieb GS, Miller AD. Retrovirology. 2010 Aug 31;7(1):70. Department of Pathology, University of Washington, Seattle WA, USA.

  8. Well done, Mindy - Thank-you. May I post a link to the CFSCentral blog on

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