Effects of short-course zidovudine on the selection of nevirapine-resistant HIV-1 in women taking single-dose nevirapine.
PMID: 22492850
2012
The Journal of infectious diseases
Abstract: HIV-1 infected pregnant women administered sdNVP with or without short-course ZDV were assessed for HIV-1 mutations (K103N, Y181C, G190A, and V106M) prior to delivery and postpartum.
HIV-1 phenotypic reverse transcriptase inhibitor drug resistance test interpretation is not dependent on the subtype of the virus backbone.
Abstract: No difference in the capacity to detect resistance associated with M184V, K103N and V106M mutations was noted between the two backbones.
Table: V106M
Discussion: An assessment of the sensitivities of these two backbones to measuring resistance in the presence of the M184V, K103N, or V106M mutation was performed.
Discussion: Another minor restriction of this analysis is that the majority of recombinant viruses carried the M184V, the K103N and the V106M mutations, which provide high-level resistance to 3TC and FTC with M184V or EFV and NVP with K103N
Impact of Novel Resistance Profiles in HIV-1 Reverse Transcriptase on Phenotypic Resistance to NVP.
Introduction: There are four types of NNRTIs-resistant mutations: (1) Primary mutation: these mutations emerge earliest during therapy and cause high-level resistance to one or more NNRTIs, including K103N/S, Y181C/I/V, V106A/M, Y188L/C/H, and G190A/S/E.
K65R in subtype C HIV-1 isolates from patients failing on a first-line regimen including d4T or AZT: comparison of Sanger and UDP sequencing data.
Discussion: The Sanger results of isolates from treated patients were as expected with a predominance of M184V, numerous TAMs of pathway1 (M41L, D67N, K70R, L210W, T215Y/F) and DRMs to NNRTIs (mainly K101E, K103N, V106M, Y181C, G190A).
Frequent emergence of N348I in HIV-1 subtype C reverse transcriptase with failure of initial therapy reduces susceptibility to reverse-transcriptase inhibitors.
Abstract: RESULTS: Y181C and M184V mutations in the RT polymerase domain were associated with failure of stavudine-lamivudine-nevirapine (d4T/3TC/NVP; P < .01), and K103N, V106M, and M184V with failure of d4T/3TC/efavirenz (EFV; P < .01).
High rate of K65R for antiretroviral therapy-naive patients with subtype C HIV infection failing a tenofovir-containing first-line regimen.
Result: According to the comments given by Stanford University HIV-1 Resistance Database, mutations V106M and Y181C can cause high level resistance to NVP, while mutations A98G and V108I just result in low-level reduction in susceptibility to NVP.
Result: Among them, I178M appeared in four parallel cultures, while V106M was selected in three independent virus cultures together with I178M.
Result: As summarized in Table 3, two reported mutations V106M and Y181C were characterized to be associated with high level of NVP resistance, while the other 5 known mutations A98G, K238N
Comparison of predicted susceptibility between genotype and virtual phenotype HIV drug resistance interpretation systems among treatment-naive HIV-infected patients in Asia: TASER-M cohort analysis.
Result: Among the 1226 patients with no discrepancy, the efavirenz-associated mutations were A98G (0.3%), K103N (0.8%), K103S (0.2%), V106M (0.2%), V179D (0.6%), Y181C (0.6%), G190A (0.3%), G190E (0.1%), P225H (0.2%), F227C (0.1%) and K238T (0.1%).
Baseline-transmitted V106V/I/M non-nucleoside reverse transcriptase inhibitor resistance in HIV-1 subtype B infection.
Abstract: V106M mutation is not often observed as a primary resistance mutation in patients infected with HIV-1 subtype B.
Abstract: The V106V/I/M mutation represents a mixture of virus strains conferring resistance to the non-nucleoside reverse transcriptase inhibitor antiretrovirals efavirenz and nevirapine.
Abstract: We report a case in which an antiretroviral therapy (ART)-naive patient diagnosed with HIV-1 subtype B presented with baseline genotype and phenotype resistance tests, confirming a V106V/I/M nucleoside resistance mutation.
Failure of initial therapy with two nucleosides and efavirenz is not associated with early emergence of mutations in the C-terminus of HIV-1 reverse transcriptase.
PMID: 21350368
2011
Journal of acquired immune deficiency syndromes (1999)
Discussion: Other known polymerase domain mutations were not significantly associated with failure although, there were possible trends for K65R (p=0.13) and V106I/M (p=0.13).
HIV mutation literature information.
PMID: 
2012
The Journal of infectious diseases
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