Susceptibility of the Human Retrovirus XMRV to Antiretroviral Inhibitors

ballard

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Can someone get access to the above article and tell us what is says.
It is by Dusty Miller from the Fred Hutchinson Cancer Center in Seattle on Medscape.
 
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Just a quick skim of 6 pgs or so of continual techno-jargon.... In laymen's terms... they have ID'd a broader range of potential antiretrovirals/ candidate Rxs than previously "appreciated"... made other important discoveries.. technical hows of inhibition, receptor sites, etc.. Their analysis resolves disparities among earlier reports... (Rxs thought to be resisted - which in adequate amt X is not resistant to) So... to rephrase their statement, i.e. not violate copyright...just in case X is found to be the culprit/disease causing in humans... there are now more Rxs from which to choose. I did not see mention of CFS specifically..... (induced infection of) breast cancer cells/ and prostate were mentioned... unless I missed something. Also the triple therapy Dr Jamie & dtr are using apparently were shown not to be very effective in other earlier studies.. but ARE in fact, if dosage is adjusted.
 
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http://www.retrovirology.com/content/7/1/70
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.
 
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Thanks for posting this. I am excited at the tantalizing possibility of one day feeling better! I know it will be awhile before we have anything that looks like a generally approved protocol, but if this illness hasn't taught me patience, it hasn't taught me anything :)