Current antiretroviral drugs can be divided into three classes:
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Nucleoside analogue reverse transcriptase inhibitors (NRTIs) were the first type of drug available to treat HIV infection in 1987. When HIV infects a cell, it copies its own genetic code into the cell's DNA, and the cell is then programmed to create new copies of HIV. To reproduce, HIV must first convert its RNA into DNA using the enzyme reverse transcriptase. Nucleoside analogue reverse transcriptase inhibitors act like false building blocks and compete with the cell's nucleosides, thereby preventing DNA synthesis. This inhibits reverse transcriptase, which prevents HIV from infecting cells and duplicating itself.
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Nonnucleoside reverse transcriptase inhibitors (NNRTIs) started to be approved in 1997. Like nucleoside analogue reverse transcriptase inhibitors, nonnucleosides also interfere with HIV's ability to infect cells by targeting reverse transcriptase. In contrast to nucleoside analogue reverse transcriptase inhibitors, nonnucleosides bind directly to the enzyme. This blocks the binding site of the reverse transcriptase and inhibits the binding of nucleotides.
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Protease inhibitors (PIs) were first approved in 1995. PIs interfere with viral replication by binding to the viral protease enzyme and preventing it from processing viral proteins into their functional forms and thereby rendering the resulting viral particles non-infectious (Peiperl, Coffey, and Volberding 2005).
Source: Authors.
