By Sudipta Bardhan-Quallen
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N 36 New Weapons Against HIV 37 Stopping the Cycle In 1985, Dr. Hiroaki Mitsuya of the NIH demonstrated that the drug AZT was able to inhibit the replication of retroviruses, the family of viruses that HIV belongs to, at least in laboratory cultures. Mitsuya believed that AZT could also be effective in human AIDS patients. AZT represents the first of a class of drugs known as nucleoside reverse transcriptase inhibitors (NRTIs). These drugs control HIV by interfering with the action of proteins essential to the virus’s life cycle.
Interestingly, there seems to be a correlation between the level of viral concentration during latency and the length of the dormant period: the higher the concentration of blood HIV in latency, the more rapidly the patient will progress to AIDS. 34 AIDS The point at which doctors say an HIV infection has turned into AIDS is defined by a patient meeting criteria set by the CDC. According to the CDC’s current definition, a person is considered to have AIDS when he or she tests positive for HIV and has either a helper T cell count of less than two hundred cells per milliliter of blood (normal levels are between five hundred and eighteen hundred) or has at least one opportunistic infection.
Since then, four other protease inhibitors have been approved: ritonavir, indinavir, nelfinavir, and amprenavir. Scientists initially thought that these drugs could do more than simply slow replication, as AZT and other NRTIs did, and stop HIV from replicating altogether. At first, the results looked promising. A 1996 study using ritonavir showed that over the seven months of the drug trial, the death rate due to AIDS was cut in half when ritonavir was administered. Unfortunately, the effects were temporary, just as they had proven to be for NRTIs.