Most antiviral drugs target viral replication by interfering with viral nucleic acid synthesis or late protein synthesis. They require conversion to active triphosphate forms by host cell kinases to inhibit viral polymerases more selectively than host polymerases. Combination antiviral therapy increases effectiveness and delays drug resistance emergence. Current HIV treatment involves two or three drugs before symptoms, often two reverse transcriptase inhibitors plus a protease inhibitor to slow viral load increases and delay resistance.