Currently, there no cure for AIDS, and moreover, no single drug has been found to suppress HIV for long. HIV replicates its DNA through reverse transcription, a process that creates a complementary strand of DNA to HIV’s viral RNA. Unlike human cells, the virus has no enzymes that proofread DNA sequences. Inevitably, a lot of mutations occur. If a single drug were used to treat AIDS, the AIDS virus would quickly mutate and become resistant to the drug. Today, a combination antiviral therapy, called HAART, uses many different types, or classes, of anti-retrovirals to stop HIV before it can reproduce and mutate.

Please click on the tabs to view these different classes.

The first two classes consist of nucleoside analogue reverse transcriptase inhibitors (NARTIs) and Non-nucleoside reverse transcriptase inhibitors (NNRTIs). To reproduce, HIV must first use reverse transcription to convert its RNA into DNA.

NARTIs provide analogues to DNA nucleotides that are missing the 3'-hydroxyl group. The hydroxyl group is the part of a nucleotide that allows other nucleotides to join and create a chain. The analogues compete with normal DNA nucleotides for incorporation into the viral DNA chain. Once it joins, with no place for other nucleotides to bind, the chain terminates and the viral replication fails.

NNRTIs take a more direct approach. They bind at different locations of the reverse transcriptase enzyme. Because the enzyme domains can no longer move, reverse transcription can no longer occur.

Other common classes of treatment include protease and integrase inhibitors, PIs and IIs. The basis of these two treatments is to block active sites of enzymes necessary for the function of HIV.

For HIV to sustain itself in a cell, it must create proteins that bind to membrane proteins of its target cells. HIV genes code for long polyproteins that must be cut by protease to create functional binding proteins. Because PIs bind to protease, protease can no longer function, leaving only harmless polyproteins behind.

To code for proteins, HIV must first have the viral genome incorporated into the human genome. The gene integrase accomplishes this. IIs bind to integrase, ending HIV’s ability to integrate into the genome.

The newest approved HIV treatment comes in the form of fusion inhibitors. To gain entry into the human cell, HIV must have surface proteins that bind to the human cell’s surface receptors. Fusion inhibitors prevent this from happening. They block proteins on both HIV and the human cell, impeding HIV’s entry into the cell.