HIV-1 is an RNA virus that infects cells and is then converted to complementary DNA (cDNA) by the action of the viral reverse transcriptase (RT). RT has little proofreading capacity and therefore incorporates errors in the proviral DNA. These errors are transcribed into infectious viral particles when the proviral DNA is transcribed into RNA. Similarly, the enzyme protease (PR) catalyzes a polyprotein to produce peptides necessary for active viral replication. Although HAART (combinations of nucleoside analogs, nonnucleoside agents, protease inhibitors and/or integrase strand transfer inhibitors) may be effective in reducing viral load, genotypic mutations arising in drug-targeted HIV loci due to selective pressure from antiviral therapy can result in antiviral resistance that may compromise such therapy.

Detectable HIV-1 genotypic mutations conferring resistance to an antiviral drug are reported as amino acid codon changes (eg, N155H), along with associated resistance interpretations for the current FDA-approved integrase strand transfer inhibitors (dolutegravir, elvitegravir, and raltegravir). Interpretation for resistance to bictegravir is not available at present.