Table 1.
Mutation status | Nonsynonymous gene mutations found in the PR gene | Known resistance to PI drugs | Level of drug resistance to protease inhibitors |
---|---|---|---|
WT | None | None | None |
M7 | V32I, L33I, M36I, I54 V, A71 V, G73S, L90 M | IDV, SQV, RTV, NFV, ATV (APV, FOS, LPV, TPV) | Low |
M10 | L10I, I13 V, K20R, L33I, M36I, I54 M, A71T, G73S, I84 V, L90 M | APV, FOS, IDV, SQV, RTV, NFV, ATV, TPV (LPV) | High |
M11 | L10F, L33F, M46I, I54L, H69 K, A71 V, G73S, V77I, V82T, I84 V, L90 M | APV, FOS, IDV, SQV, RTV, NFV, ATV, TPV (LPV) | High |
The three mutant HIV-1 PRs were isolated from the plasma samples of HIV-infected patients who were cared at the University of Maryland Medical Center. They carried seven (M7), ten (M10) and eleven (M11) PR gene mutations, respectively. The wildtype (WT) PR was derived from pNL4-3. The drug resistant profiles were generated in a CAP/CLIA accredited hospital laboratory as part of the clinical reports by using the ViroSeq HIV-1 Genotyping System (Abbott Molecular, Chicago, IL). APV, Amprenavir; FOS, Fosamprenavir; IDV, Indinavir; SQV, Saquinavir; LPV, Lopinavir + Ritonavir; RTV, Ritonavir; NFV, Nelfinavir; ATV, Atazanavir; TPV, Tipranavir; Drugs in parenthesis indicate possible drug resistance