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“It’s the Faucet, Stupid.” Comparing something called telomere lengths of CD4+ and CD8+ T lymphocytes in HIV-infected and uninfected persons, Amsterdam’s Frank Miedema et al. claim “there is no evidence for increased turnover of CD4+ T cells in HIV infection.” Miedema’s provocative paper (Science 274,1543) concludes that, rather than destroying the body’s CD4+ T cells (as Ho would have it), HIV instead prevents the production of T cells — the “tap,” not the “drain.” The Aaron Diamond team insists that the preponderance of evidence favors the “drain” model.

“Genomic Resistance Doesn’t Matter.” Contrary to the conventional wisdom, R. Tedder, member of the Delta virology team, reports that resistance to AZT actually developed more quickly on the AZT+ddI and AZT+ddC combination arms than it did in the AZT monotherapy arm — and that the development of drug resistant mutants didn’t affect clinical outcome. “Genomic resistance doesn’t matter,” he asserted, “instead, it is the amount of resistant virus that matters.” “Let’s use resistance information in the most general terms,” he challenged his U.K. audience, “that is, as it is reflected in rises in plasma RNA.”

T-cell Tropic (SI) Virus Independently Predicts Progression to AIDS or Death. Meanwhile, the ACTG 175 virology team, led by Stanford’s David Katzenstein, reports that the HIV viral phenotype (T-cell tropic (“SI”) vs. macrophage tropic (“NSI”)) at baseline was independently predictive of clinical outcome in the ACTG’s AZT/ddI/ddC mega-trial. With a relative risk ratio (SI present at study entry/SI absent at study entry) of .40, the risk of progressing to new disease or death is reduced 60% for persons with an NSI viral phenotype at baseline versus an SI.

“Undetectable” on Delta. Also from the Delta virology team, investigators report that in study volunteers with no previous antiretroviral treatment (“naive”), the drug regimens AZT, AZT+ddI and AZT+ddC reduced HIV RNA plasma viral load to below the lower limit of detection of the assay (quaintly referred to as “undetectable”) in 10%, 40% and 20%, respectively, of study participants. Maybe “undetectable” is not such a big deal after all. (Seems it’s all about durability…)

Hit it Early, Hit it — with nevirapine? Dr. Brian Conway, principal investigator of the INCAS study, upon presenting his AZT+ddI+nevirapine data which reduced plasma viral load to < 500 copies in 60% of patients at 6 months (AZT+ddI did the same thing in 30% of patients), asks, “Do we really want to hit early and hard — or just early with a regimen that will get the job done?” Oddly, after presenting follow-up data showing that, even in compliant patients, resistance to nevirapine and AZT begins to emerge at 12 months, he seems to have answered his own question.

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