Infections

Deaths from AIDS in the U.S. have dropped sharply since 1995 when a potent set of drugs called protease inhibitors became available (Seppa, 1998). Protease inhibitors strengthen the body's immune system by keeping HIV, the AIDS virus, from replicating itself and increasing the number of virus-fighting T cells, cells of the immune system which kill the virus, in the blood. Protease inhibitors have proved especially effective when used in combination with other anti-HIV medications. Such drug combinations have helped slow the rate at which HIV-positive people develop AIDS and have reduced the number of AIDS-related deaths in the U.S. from 21,460 in the first half of 1996 to 12,040 in the

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g Crixivan(R) (indinavir), resulted in marked decreases in viral RNA and increases in CD4 cell counts. Ritonavir has the disadvantage of raising and lowering the levels of many other drugs through its effect on the liver. However, several reports have shown that ritonavir is particularly attractive in dual protease inhibitor regimens, with demonstrable synergistic anti-HIV effects Henderson, 1998, p. 1). Saquinavir may be more easily tolerated but it is poorly absorbed and thus is not as effective in its currently available form. Data from long-term non-progressors - individuals who remain asymptomatic despite HIV infection of 10 years or more - suggests that early treatment allows control of the virus, and that the pattern of low virus load and normal T-cell counts seen in patients treated early with highly effective antiretroviral therapy regimens is similar to that seen in the long-term non-progressors. There is also evidence that early, aggressive treatment is associated with a survival advantage over delayed treatment. These findings led researchers to use combinations of protease inhibitors. Saquinavir, a peptidomimetic HIV protease inhibitor, has been shown to be effective in reducing patient viral load and reduci
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Approximate Word count = 3989
Approximate Pages = 16 (250 words per page)

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