Method: The final list of mutations included M41L, E44D, D67N, T69D, K70R, L74V, L100I, K103N, V108I, V118I, Y181C, M184V, G190A, L210W, T215F, T215Y and K219Q in RT; and L33F, L33I, M46I, M46L, G48V, <
HIV-1 protease mutations and protease inhibitor cross-resistance.
PMID: 20660676
2010
Antimicrobial agents and chemotherapy
Abstract: Of the mutations with the greatest effect on PI susceptibility, I84AV was associated with decreased susceptibility to eight PIs; V32I, G48V, I54ALMSTV, V82F, and L90M were associated with decreased susceptibility to six to seven PIs; I47A, G48M, I50V, L76V, V82ST, and N88S were associated with decreased susceptibility to four to five PIs; and D30N, PMID: 18992847
2009
Infection, genetics and evolution
Abstract: V82L mutation was present with increased frequency in isolates from children compared to isolates from adults infected with both subtypes.
Result: Only V82L was present with increased frequency in subtype B (6.7%) and F1 (8.3%, not shown) isolates from children compared to subtype B (0%) and F1 (0.8%) isolates from adults (Table 2).
Table: V82L
Discussion: Interestingly, V82L reported by IAS consensus as a major mutation specifically associated with resistance to tipranavir, not used by our cohort, was observed in subtypes B and F1 isolated from treated children but not in adults.
The prevalence of resistance-associated mutations to protease and reverse transcriptase inhibitors in treatment-naive (HIV1)-infected individuals in Casablanca, Morocco.
PMID: 19759509
2009
Journal of infection in developing countries
Abstract: Only two major mutations, M46L and V82L, were separately found in three individuals of 71 (4.2%) with one carrying both mutations.
Population trends in the prevalence and patterns of protease resistance related to exposure to unboosted and boosted protease inhibitors.
Abstract: Individual mutations L33F, M461/L, V82A/F/T/S/L and 184V became relatively more frequent over the period of study.
Genotypic resistance profile and clinical progression of treatment-experienced HIV type 1-infected patients with virological failure.
PMID: 18240962
2008
AIDS research and human retroviruses
Abstract: In multivariable models adjusting for prior AIDS, baseline CD4 counts, HIV-1 RNA, and calendar year, viral resistance variables associated with increased hazards of clinical progression were the presence of reverse transcriptase substitution T215F (p = 0.002) and the presence of three or more protease substitutions among L33F/I/V, V82A/F/L/T, I84V, and L90M (p = 0.003).
Characterization of a novel human immunodeficiency virus type 1 protease inhibitor, A-790742.
PMID: 18212102
2008
Antimicrobial agents and chemotherapy
Abstract: During in vitro selection, A-790742 selected two primary mutations (V82L and I84V) along with L23I, L33F, K45I, A71V/A, and V77I in the pNL4-3 background and two other mutations (A71V and V82G) accompanied by M46I and L63P in the HIV-1 RF background.
Abstract: HIV-1 pNL4-3 clones with a single V82L or I84V mutation were phenotypically resistant to A-790742 and ritonavir.
Abstract: The selection of the uncommon V82L and V82G mutations in
Impact of the number of failed therapeutic regimes on the development of resistance mutations to HIV-1 in northeast Brazil.
PMID: 17962868
2007
The Brazilian journal of infectious diseases
Abstract: There was a significant increase in resistance mutations V82A/F/L/T, I84V, L90M, M41L, K70R, L210W, T215Y/F and K219Q/E in MF.
Tipranavir: a new protease inhibitor for the treatment of antiretroviral-experienced HIV-infected patients.
PMID: 17425479
2007
Expert opinion on pharmacotherapy
Abstract: The TPV mutation score includes L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D and I84V.
HIV mutation literature information.
PMID: 
2011
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