Results for a 15 drug panel are reported as comparative drug susceptibility with IC 50 for each drug. The goal of therapy with these agents is to continuously inhibit viral replication. The measurement of HIV-1 RNA levels, or viral load, is used along with CD4 measurements to monitor treatment efficacy. The selection of mutant HIV-1 viruses is favored by the high error rate of the viral reverse transcriptase enzyme and by the high replication rate of the virus. It is estimated that the combination of these factors leads to the generation of every possible single drug resistance mutation in a viral population each day.
Some mutations are lethal and completely inhibit further viral replication.
Other mutations may cause amino acid changes in viral proteins at sites essential for function, including antiviral drug-binding sites, and can result in reduced susceptibility to therapy, leading to treatment failure. In general, wild type virus is best adapted for replication in the host and mutations that lead to drug resistance often reduce the fitness or replicative ability of the virus, leading to lower replication rates in the absence of drug. However, in the presence of antiretroviral drugs, the mutated virus may have selective advantage and can become the dominant species. The two general types of mutations that arise during HIV-1 infections are generally identified as primary and secondary. Primary mutations are fairly specific for each drug and appear shortly after the start of drug treatment.