Study of antiretroviral mutants in HIV patients with treatment failures and the effect of risk factors in the virological failures.
PMID: 16553322
2005
Revista do Instituto de Medicina Tropical de Sao Paulo
Abstract: The most frequent mutations were M41L, M184V, and T215FY in RT and L62PI, L10FIRV and M36I in PT.
Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.
PMID: 19825125
2005
Journal of the International AIDS Society
Table: M36I
Decrease of replicative capacity of HIV isolates after genotypic guided change of therapy.
Abstract: After the change of therapy, an increase in the number of drug resistance mutations in the protease gene was detected in both groups with a higher prevalence of M36I mutation in immune responders.
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%).
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.
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: Significant differences were found in the rates of M36I (98 and 36%), L63P (35 and 59%), A71V (3 and 32%), V77I (0 and 36%), and I93L (91 and 32%) (0.0001 < P < 0.05) in C and B, respectively.
Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.
Abstract: the subtype B mutant, with mutations Q7K, S37N, R41K, K45R, I54V, L63P, A71V, V82A and L90M, and the subtype F (wild type), naturally carrying mutations Q7K, I15V, E35D, M36I, S37N, R41K, R57K, D60E, Q61N, I62V, L63S, I64L and L89M, with res
Comparing the accumulation of active- and nonactive-site mutations in the HIV-1 protease.
Abstract: This variant possessed the ritonavir-resistance-associated mutations in the active-site (V32I and V82A) and nonactive-site mutations (K20R, L33F, M36I, L63P, A71V, and L90M).
Impact of frequent natural polymorphisms at the protease gene on the in vitro susceptibility to protease inhibitors in HIV-1 non-B subtypes.
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.