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STI stands for “structured treatment interruptions,” but it could just as easily stand for “stop taking it” (“it,” in this case, being one’s HIV medication). The concept goes against just about every doctor’s admonition you’ve ever heard—yet in one instance, at least, it seems to work.
    In a new study by scientists at the Wistar Institute and elsewhere at Penn, drug-treatment interruptions have, for the first time, been shown to boost HIV-specific immune responses in chronically infected patients. The idea behind the STI treatment is that once a patient has been taking a “cocktail” of three or four powerful—and often debilitating—virus-suppressing drugs, a controlled “stop-and-start” strategy of drug treatment can coax the immune system into developing an increasing capacity to control HIV infection.
    During the “observational study,” 10 AIDS patients were monitored: five had interrupted their medication at their own discretion for a median period of eight weeks, while the other five were not on any medication. All five patients in the experimental group showed significant increases in anti-HIV responses during the interruption periods. A report on the study appeared in the September issue of the Journal of Infectious Diseases, and volunteers are being recruited to test the concept
in a clinical trial.
    Dr. Luis J. Montaner, the assistant professor at the Wistar Institute and adjunct assistant professor of microbiology at the School of Veterinary Medicine who served as the study’s senior author, said that although HIV would “likely not be eradicated in these patients,” he expects the virus to be “fully controlled by the immune system without the toxicity associated with current drug therapies.”
    This approach is not without risks, notes Dr. Jay Kostman, head of the Division of Infectious Diseases at Presbyterian Medical Center and principal clinician for the trial, who adds that the team will be carefully monitoring such potential side effects as “the emergence of viral resistance or an acceleration of disease progression.”

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