Super science (beyond superbugs) from the Conference on Retroviruses and Opportunistic Infections (CROI)
When researcher David Ho, MD, unleashed a media frenzy in February by
announcing that a gay New York City man had contracted a multi-drug
resistant, fast-progressing HIV strain (see “Big, Bad Media Bugout"), few doubted that he’d grab headlines two weeks later in Boston
at CROI, the year’s top AIDS confab. The hoopla unfortunately
overshadowed “the best [CROI] in years in terms of therapy progress,”
says Project Inform’s Marty Delaney. Check these future features:
PROTEASE PROMISE In Phase III trials, long-anticipated protease inhibitor (PI) tipranavir—the
FDA will likely approve it this summer—performed better in
protease-resistant HIVers than PI rivals like Kaletra. Tibotec’s PI
contender TMC-114 may prove even more promising. In a large, six-month Phase II study of multidrug-resistant
HIVers, TMC-114 combos smashed viral load on average by nearly two logs
(say, from 60,000 to 600)—even to undetectable at the highest dose.
NON-NUKE NOTES Over a year, adding Pfizer’s non-nuke capravirine
to a PI-plus-two-nukes combo didn’t suppress non-nuke-resistant HIVers’
viral loads better than the combo without capravirine. But Tibotec
scored again with non-nuke TMC-278, plunging viral loads in seven days. Larger TMC-278 trials start this spring.
NEW CLASSES Drugs that stop HIV in novel ways are a-brewin’. For nine days, a single dose of Panacos’ maturation inhibitor PA-457—which blocks the same HIV step as PIs, but differently—dropped viral loads significantly. And in a tiny trial, Merck’s integrase inhibitor L-870810—which
keeps HIV from stuffing its own DNA into human DNA—cut HIVers’ viral
loads over 10 days of twice-daily dosing. Too bad toxicity in dog
studies has shelved it, though Merck plans to proceed with a similar
compound. Woof!
