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New drug offers promise in treating HIV

New drug offers promise in treating HIV

Offering a promising new way to attack HIV, research on monkeys suggests that an experimental drug helps keep HIV in check by blocking an enzyme that is crucial to infection. The target is integrase, an HIV enzyme that the virus needs to hijack a patient's cells and spread. Repeated attempts to inhibit integrase's function and stall the virus have failed. But Merck researchers reported Thursday in the journal Science that they have developed an integrase inhibitor that significantly protected monkeys when given early in infection and provided some benefit to the very sick as well. Merck is now studying some integrase inhibitor candidates in a handful of people to see whether the pills seem safe and to check for any early signs of viral suppression. Results, due early next year, will determine whether larger studies should be performed on any of the prospective inhibitors. Far more research is needed, but the monkey results have leading AIDS researchers watching closely to see whether it might finally be possible to attack integrase. Anthony Fauci, who heads the National Institute of Allergy and Infectious Diseases, cautioned that he wasn't "doing cartwheels over this," but said, "This is the next step in the process that the field, myself included, has been looking for for some time now. It's a very important target." Integrase is crucial to the melding of HIV genes with patients' own DNA. Fauci said that step is key to HIV's sneakiest trait--its ability to hide inside cells so it can rebound after therapy. But blocking integrase has proved notoriously difficult. Just last year GlaxoSmithKline and Japan's Shionogi abandoned one experimental integrase inhibitor after initial human studies, going back to the lab to search for stronger candidates. Merck researchers gave their candidate, code-named L-879812, to six monkeys newly infected with a combination monkey-human version of HIV. The animals experienced only a mild decrease in crucial immune cells called CD4s, and four had their virus drop to undetectable levels, lead researchers Daria Hazuda and Steven Young report. In contrast, six untreated monkeys saw their CD4-cell levels plummet and viral levels soar. Almost three months later Hazuda treated those monkeys, who by then had become very ill. All improved somewhat but didn't rebound nearly as well or for as long as the newly infected monkeys. Hazuda said drug-caused viral suppression apparently worked more in concert with a monkey's immune system when it hadn't yet been ravaged, allowing the body a greater capacity to fight back. (AP)

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