Mutation D30N is not preferentially selected by human immunodeficiency virus type 1 subtype C in the development of resistance to nelfinavir.
PMID: 15155216
2004
Antimicrobial agents and chemotherapy
Abstract: Other mutations were L10I/V, K20R, M46I, V82A/I, I84V, N88D, and N88S.
Comparison of drug resistance mutations and their interpretation in patients infected with non-B HIV-1 variants and matched patients infected with HIV-1 subtype B.
PMID: 15097148
2004
Journal of acquired immune deficiency syndromes (1999)
Abstract: In the protease gene, differences between patients infected with B or non-B strains were mainly observed for mutations playing a minor role in drug resistance and known to occur mainly as a natural polymorphism in non-B strains: K20R/M/I, M36I, L63P, A71V/T, and V77I.
Protease mutations in HIV-1 non-B strains infecting drug-naive villagers in Cameroon.
PMID: 15008125
2004
AIDS research and human retroviruses
Abstract: Secondary PI resistance-associated mutations were identified at five sites: L10I/V (16%), K20R (8%), M36I (98%), L63P (13%), and V77I (6%).
HIV-1 phenotypic susceptibility to lopinavir (LPV) and genotypic analysis in LPV/r-naive subjects with prior protease inhibitor experience.
PMID: 12869832
2003
Journal of acquired immune deficiency syndromes (1999)
Abstract: Current PI therapy (P = 0.002) and indinavir administration (P < 0.001), >5 LPV/r mutations (P < 0.0012), and detection of L10FIRV, K20MR, M46IL, I54VL, A71VT, G73SA, V82AFTS, I84V, and M90L were associated with LPV resistance in univariate analysis.
Abstract: Factors independently associated with LPV resistance were K20MR (odds ratio [OR], 13.9; 95% confidence interval [CI], 1.3-145.1; P = 0.028), I54VL (OR, 131.7; 95% CI, 10.5-1654.7; P < 0.001), G73SA (OR, 19.2; 95%
Genotypic inhibitory quotient as predictor of virological response to ritonavir-amprenavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients.
PMID: 12543665
2003
Antimicrobial agents and chemotherapy
Abstract: Baseline PI resistance mutations (L10F/I/V, K20M/R, E35D, R41K, I54V, L63P, V82A/F/T/S, I84V) identified by univariate analysis and included in a genotypic score and APV C(min) at week 8 were predictive of the virological response at week 12.
Rates of transmission of antiretroviral drug resistant strains of HIV-1.
Abstract: Accessory mutations were found in the PR gene at the following positions: L63P/V/T/A/I [153/345 (44.3%)], M36I/L [149/345 (43.2%)], L10I/F/V [82/345 (23.8%)], V77I [60/345 (17.4%)], A71V/T [11/345 (3.2%)], K20M/R [10/345 (2.9%)], and V82I [4/345 (1.2%)].
Identification and distribution of HIV type 1 genetic diversity and protease inhibitor resistance-associated mutations in Shanghai, P. R. China.
PMID: 14501800
2003
Journal of acquired immune deficiency syndromes (1999)
Abstract: Substitutions characteristic with the subtype B/B' sequences mainly among hemophiliacs included L63P (87%), A71V/T (27%), and V77I (93%) while those that characterized the non-B sequences mainly found among heterosexuals included M36I (69%) and K20R (19%).
Testing genotypic and phenotypic resistance in human immunodeficiency virus type 1 isolates of clade B and other clades from children failing antiretroviral therapy.
PMID: 12454144
2002
Journal of clinical microbiology
Abstract: Prevalence of known drug resistance mutations revealed slightly significant differences among B and non-B subtypes: L10I, 21 and 64%, K20R, 13 and 43%, M36I, 34 and 100%, L63P, 76 and 36%, A71V/T, 24 and 0%, and V77I, 32 and 0%, respectively, in the protease (0.0001 D67N, 38 and 8%, K70R, 33 and 0%, R211K, 49 and 85%, and K219Q/E, 31 and 0%, respectively, in the reverse transcriptase (0.0256
Resistance testing in children changing human immunodeficiency virus type 1 protease inhibitor.
PMID: 12005085
2002
The Pediatric infectious disease journal
Abstract: K20R/I) conferred by primary (active site) resistance mutations.
HIV mutation literature information.
PMID: 
2004
Antimicrobial agents and chemotherapy
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