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 HIV mutation literature information.


  Virologic rebound on HAART in the context of low treatment adherence is associated with a low prevalence of antiretroviral drug resistance.
 PMID: 12131564       2002       Journal of acquired immune deficiency syndromes (1999)
Abstract: In the viremic group, substitutions in HIV protease were detected most frequently in the following positions in subjects on indinavir (IDV): L10I/V (35.7%), M46I/L (35.7%), A71T/V (35.7%), V82A (42.9%); and for subjects on nelfinavir (NFV): D30N (50.0%), V77I (56.3%), N88D (37.5%).


  Virologic response to nelfinavir-based regimens: pharmacokinetics and drug resistance mutations (VIRAPHAR study).
 PMID: 12131209       2002       AIDS (London, England)
Abstract: At failure, L10I, D30N, M36I, V77I, N88S/D or L90M protease mutations had emerged since baseline.


  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).


  Analysis of HIV-1 drug resistant mutations by line probe assay and direct sequencing in a cohort of therapy naive HIV-1 infected Italian patients.
 PMID: 11737863       2001       BMC microbiology
Result: In particular, the most frequent substitutions, by genotyping analysis, are present at codon 36 [M36I alone (7 cases) or associated with L10V (2 cases)], at codon 63 [L63P alone (5 cases) or associated with V77I (2 cases)] and at codon 77 [V77I (5 cases)], while L10V was always found in association with A71V or M36I.


  Genotypic variation of HIV-1 reverse transcriptase and protease: comparative analysis of clade C and clade B.
 PMID: 11504976       2001       AIDS (London, England)
Abstract: RESULTS: There were 87 clade B (14 naive) and 78 clade C (20 naive) [corrected] with significant differences in the prevalence of known drug-resistance mutations between the clades: in naive patients in the protease region M36I 7% and 95% (P < 0.0001), K20R 0% and 27% (P = 0.063), A71V 18% and 0% (P = 0.063), M46I 0% and 13%, and V77I 18% and 0% (P = 0.063), respectively, and in the reverse transcriptase region A98G/S 0% and 20% (P = 0.12), respectively.
Abstract: There were also significant differences (P < 0.03 to < 0.0001) in treated patients in clades B and C: in the protease region L10I 40% and 12%, M3


  Genetic diversity of protease and reverse transcriptase sequences in non-subtype-B human immunodeficiency virus type 1 strains: evidence of many minor drug resistance mutations in treatment-naive patients.
 PMID: 11060045       2000       Journal of clinical microbiology
Abstract: In order of decreasing frequency, the following mutations were identified in the protease gene: M36I (86.6%), L10I/V (26%), L63P (12.6%), K20M/R (11.2%), V77I (5.6%), A71V (2.8%), L33F (0.7%), and M46I (0.7%).


  Susceptibility to PNU-140690 (Tipranavir) of human immunodeficiency virus type 1 isolates derived from patients with multidrug resistance to other protease inhibitors.
 PMID: 10770770       2000       Antimicrobial agents and chemotherapy
Abstract: The substitutions among the amino acid residues of the protease included L10I, K20R, L24I, M36I, N37D, G48V, I54V, L63P, I64V, A71V, V77I, V82A, I84V, and L90M.



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