Reconsidering Early HIV Treatment and Supervised Treatment Interruptions 英文参考文献.docVIP

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Reconsidering Early HIV Treatment and Supervised Treatment Interruptions 英文参考文献.doc

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Reconsidering Early HIV Treatment and Supervised Treatment Interruptions 英文参考文献

Open access, freely available online Perspectives Reconsidering Early HIV Treatment and Supervised Treatment Interruptions Richard A. Koup T he devastating effects of HIV infection worldwide are reason enough for AIDS researchers to grasp at thin rays of hope. But seldom has a single anecdotal case stimulated as much hope as the 1999 report of an acutely infected patient who appeared to control HIV replication after two short treatment interruptions [1]. This report generated the HIV infection and supervised treatment interruptions (STIs) as a way to boost the immune response. Several small trials of STIs in chronically infected patients were carried out [4], buoyed by the reasonable desire of patients for respite from the unpleasant side effects of the drugs. These trials gave disappointing results, up to and including the hypothesis that early antiretroviral treatment (during or very soon after symptomatic seroconversion) allows the incompletely damaged immune system to recover and respond appropriately to virus antigens during treatment interruptions. This, in turn, according to the hypothesis, leads to control of viral replication by a healed and appropriately stimulated immune response to the patient’s HIV infection. Consistent with this hypothesis emergence of antiretroviral drug resistance in patients randomized to receive STIs. HIV-speci?c immune responses did increase off therapy, but so did viral loads. The so-called immune boosting probably re?ected an immune response to greater viral antigen load but did not represent constructive immune enhancement. Larger trials clearly showed that STIs were of little if any bene?t in chronic infection and that when therapy was stopped, viral loads invariably returned to pre-treatment levels [5]. Other studies indicated that HIV-speci?c CD4+ T cells were being preferentially infected, often massively, during treatment interruptions [6], and that proliferative responses were more likely to be a consequence—rather