Abstract: CONCLUSION: Collectively, these data indicate that genetic variation at NNRTI resistance-associated positions such as V106M and A98S is substantially greater in subtype C-infected patients than in subtype B-infected patients.
Abstract: In NNRTI experienced patients, the number of A98G/S changes was significantly higher in subtype C patients treated with either efavirenz or nevirapine (P < 0.0001), and V106M was higher in efavirenz-treated subtype C-infected patients (P < 0.0001).
Baseline-transmitted V106V/I/M non-nucleoside reverse transcriptase inhibitor resistance in HIV-1 subtype B infection.
Abstract: CONCLUSIONS: V106M may be a signature mutation in clade C patients treated with EFV and may have the potential to confer high-level multi-NNRTI resistance.
Abstract: Cell-based phenotypic assays were performed to determine the effects of V106M and V106A on levels of resistance to EFV, nevirapine and delavirdine.
Abstract: Generation of V106M recombinant viruses by site-directed mutagenesis confirmed the ability of V106M to confer NNRTI cross-resistance.
Abstract: In current genotypic interpretative reports (including 15 algorithmic databases), V106A is listed as an nevirapine-specific mutation while V106M is not recognized.
Abstract: M
The M184V substitution in human immunodeficiency virus type 1 reverse transcriptase delays the development of resistance to amprenavir and efavirenz in subtype B and C clinical isolates.
PMID: 12821504
2003
Antimicrobial agents and chemotherapy
Abstract: Genotypic analysis revealed differences in EFV resistance-conferring mutations in subtype B (K103N) versus subtype C (V106 M), and the appearance of both was significantly delayed in the M184V-containing variants compared with the wild type (WT).
Baseline-transmitted V106V/I/M non-nucleoside reverse transcriptase inhibitor resistance in HIV-1 subtype B infection.
Abstract: V106M is a novel resistance mutation found in subtype C viruses exposed to efavirenz.
Abstract: Here we describe the presence of V106M in seven out of 141 South African women (5%) 6 weeks after receiving nevirapine.
Drug resistance profiles of recombinant reverse transcriptases from human immunodeficiency virus type 1 subtypes A/E, B, and C.
PMID: 14585205
2003
AIDS research and human retroviruses
Abstract: Subtype C variants containing the novel V106M resistance codon showed cross-resistance to all approved NNRTIs in cell-free RT assays.
Genetic divergence of human immunodeficiency virus type 1 Ethiopian clade C reverse transcriptase (RT) and rapid development of resistance against nonnucleoside inhibitors of RT.
PMID: 12069959
2002
Antimicrobial agents and chemotherapy
Abstract: In the case of subtype C, selection with NVP and/or EFV led to the appearance of several previously unseen mutations in RT, i.e., V106M and S98I, as well as other mutations that have been previously reported (e.g., K103N, V106A, V108I, and Y181C).
Polymorphisms of cytotoxic T-lymphocyte (CTL) and T-helper epitopes within reverse transcriptase (RT) of HIV-1 subtype C from Ethiopia and Botswana following selection of antiretroviral drug resistance.
Abstract: Mutations within immunogenic regions of clade C RT were noted during drug selection of subtype C isolates with nevirapine (S98I, Y181C, V108I and K103N), delavirdine, (A62V, V75E, L100I, K103T, V108I, Y181C), efavirenz (K103E, V106M, V179D, Y188C/H, G190A), lamivudine (M184I, M184V), and zidovudine (K70R), respectively.
HIV mutation literature information.
PMID: 
2004
AIDS (London, England)
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