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 HIV mutation literature information.


  Association of a novel human immunodeficiency virus type 1 protease substrate cleft mutation, L23I, with protease inhibitor therapy and in vitro drug resistance.
 PMID: 15561868       2004       Antimicrobial agents and chemotherapy
Abstract: In combination with V82I, L23I was associated with a sevenfold reduction in nelfinavir susceptibility and a decrease in replication capacity.


  Impact of frequent natural polymorphisms at the protease gene on the in vitro susceptibility to protease inhibitors in HIV-1 non-B subtypes.
 PMID: 15465415       2004       Journal of clinical virology
Abstract: The first virus, which had K20I, M36I and V82I, showed 2.9-fold decreased susceptibility to APV, while the second virus showed 3.9-fold decreased susceptibility to both NFV and RTV, with amino acid substitutions K20I, M36I, L63P and V82I.


  Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.
 PMID: 15168798       2004       Antiviral research
Abstract: The frequency of the amino acid substitutions V82T/I and L90M decreased rapidly with a short half life (t(1/2) < 10 days).


  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.


  High incidence of non-B and recombinant HIV-1 strains in newly diagnosed patients in Galicia, Spain: study of genotypic resistance.
 PMID: 14518705       2003       Antiviral therapy
Abstract: In one patient (1.2%) infected with a subtype G strain, resistance-associated mutations in PR (K20I+M36I+M46I+V82I) were detected.


  Rates of transmission of antiretroviral drug resistant strains of HIV-1.
 PMID: 12600647       2003       Journal of clinical virology
Abstract: The prevalence of mutations that conferred primary resistance to protease inhibitors (PIs) was only 0.8% at position V82I.


  Brazilian Network for HIV Drug Resistance Surveillance (HIV-BResNet): a survey of chronically infected individuals.
 PMID: 12700457       2003       AIDS (London, England)
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%)].


  Low prevalence of primary mutations associated with drug resistance in antiviral-naive patients at therapy initiation.
 PMID: 11873006       2002       AIDS (London, England)
Abstract: Primary mutations associated with substantial resistance to protease inhibitors were found in only five of 347 patients (1.4%) (M46V/L, I54V, V82A/I); all the other patients carried only secondary mutations (L10F/I/V, M36I, L63P, A71T/V, V77I).


  HIV protease and reverse transcriptase variation and therapy outcome in antiretroviral-naive individuals from a large North American cohort.
 PMID: 11316997       2001       AIDS (London, England)
Abstract: However, the data suggest that some individuals (harboring a M184V mutation in RT or a V82I in protease) may have benefited from pre-therapy resistance tests.


  Molecular mechanics analysis of drug-resistant mutants of HIV protease.
 PMID: 10388843       1999       Protein engineering
Abstract: In order to study drug resistance, the wild-type HIV-1 protease and the mutants R8Q, V32I, M46I, V82A, V82I, V82F, I84V, V32I/I84V and M46I/I84V were modeled with the inhibitors saquinavir and indinavir using the program AMMP.



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