Chronic Fatigue is a common symptom in Gulf War Illness; Chronic Fatigue Syndrome is a “Presumptive” condition for Gulf War veterans
Written by Cinda Crawford
(HealthMatterShow.com) - As reported 8/31/10 in Retrovirology, researchers are seeing some success in having XMRV retrovirus react to HIV Anti-retroviral drugs for CFS. (Sorry if the link will not work. It seems to be functioning hit or miss from their end, but the information is included below. Keep reading.)
Do their conclusions mean you should spend money to get tested for XMRV right now? Probably not. Do they mean that you should consider taking anti-retroviral drugs? Truly, no. Their conclusions are not that well-defined. Not yet.
Even so… no one can walk in someone else’s shoes to feel their desperation or fading hope, but truly this seems like a premature action to me. I urge you to wait for science to catch up with the news and expectations. We will eventually have a clear picture of XMRV, but unless you want to chase every possible scenario out there, it is more prudent to wait.
(See the abstract below.)
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.
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.
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.
Best wishes for your speedy recovery from CFS, Chronic Fatigue Syndrome,
Cinda Crawford, host of the Health Matters Show