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.
A major role for a set of non-active site mutations in the development of HIV-1 protease drug resistance.
Abstract: This mutant protease contains 11 mutations, 10 of which are located outside the active site (L10I/M36I/S37D/M46I/R57K/L63P/A71V/G73S/L90M/I93L) and 1 within the active site (I84V).
Prevalence of drug-resistance-associated mutations in antiretroviral drug-naive Zambians infected with subtype C HIV-1.
PMID: 12643279
2003
AIDS research and human retroviruses
Abstract: The generated sequences revealed only secondary associated, but no primary, drug-resistance mutations The most frequent secondary mutations in the protease and RT genes were, respectively, I93L(91.7%), L89M (79.2%), M3611V (79%, 4.2%), and R211K (70.8%), S48T (62.5%).
In vitro hypersusceptibility of human immunodeficiency virus type 1 subtype C protease to lopinavir.
PMID: 12936979
2003
Antimicrobial agents and chemotherapy
Abstract: However, we did observe hypersusceptibility to lopinavir solely in clone C6, which includes the I93L substitution (a 2.6-fold decrease in the IC(50) compared to that for the subtype B reference strain).
Abstract: In order to characterize the impact of genetic polymorphisms on the susceptibility of subtype C strains of human immunodeficiency virus type 1 to protease inhibitors (PIs), a subtype B protease that originated from an infectious clone was modified through site-directed mutagenesis to include the amino acid residue signatures of subtype C viruses (I15V, M36I, R41K, H69K, L89 M) with (clone C6) or without (clone C5) an I93L polymorp
Molecular characteristics of human immunodeficiency virus type 1 subtype C viruses from KwaZulu-Natal, South Africa: implications for vaccine and antiretroviral control strategies.
Abstract: One frequent polymorphism, I93L, was located near the protease/reverse transcriptase cleavage site.
Resistance-associated mutations in the human immunodeficiency virus type 1 subtype c protease gene from treated and untreated patients in the United Kingdom.
PMID: 11427587
2001
Journal of clinical microbiology
Abstract: M36I and I93L mutations were observed in nearly all samples from both treated and untreated patients and so cannot be considered as resistance-associated mutations in this subtype.
Genotypic variation of HIV-1 reverse transcriptase and protease: comparative analysis of clade C and clade B.
Abstract: Most clade C viruses also showed significant differences from clade B consensus sequence at additional protease sites: R41K 100%, H69K/Q 85%, L89M 95% and I93L 80% (P < 0.0001).
Variant human immunodeficiency virus type 1 proteases and response to combination therapy including a protease inhibitor.
PMID: 11181376
2001
Antimicrobial agents and chemotherapy
Abstract: I93L, occurring in about 30% of untreated patients, may play a role, as A71V/T possibly does in ritonavir-treated patients.
Abstract: A relatively poorer response to therapy was associated with a high number of baseline polymorphisms and, to a lesser extent, with the presence of I93L at baseline in comparison with the wild-type virus.
Resistance-related mutations in the HIV-1 protease gene of patients treated for 1 year with the protease inhibitor ritonavir (ABT-538).
HIV mutation literature information.
PMID: 
2004
Antimicrobial agents and chemotherapy
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