Early clinical response and presence of viral resistant minority variants: a proof of concept study.
PMID: 25397504
2014
Journal of the International AIDS Society
Abstract: Single mutations E138K (two cases) and M184V in three distinct patients and V90I+G190E; M184V+A98S; Y215F+V118I+T215I; L210S+T215I+F227L; and A62V+D67G+K70N+188H in the remaining five subjects.
The lysine 65 residue in HIV-1 reverse transcriptase function and in nucleoside analog drug resistance.
Introduction: In one study, virus from 50% of patients (4/8) who developed the K65R mutation following tenofovir treatment also contained at least one of the A62V or S68G mutations; however, in all patients with the K65R virus, viremia did not return to the pre-treatment baseline, potentially reflecting the effect of K65R on viral fitness.
Introduction: Q151 is mutated to methionine (Q151M) in response to treatment with dideoxynucleoside analogs and usually occurs in combination with A62V, V75I, F77L, and F116Y mutations.
Introduction: The Q151M complex consists of five mutations ( PMID: 25259833
2014
AIDS (London, England)
Method: To limit the number of sequences, we first excluded sequences having more than one DRM (other than A62V) and having ambiguous nucleotides at more than 1% of positions.
Result: A62V, an accessory NRTI-associated mutation endemic in Russian AFSU strains, was present in 235 (78%) of 300 subtype A viruses and in one (1.8%) of 55 CRF02_AG viruses (P < 0.001).
Discussion: A second difference between subtype AFSU strains and other subtypes is the high proportion of antiretroviral-naive patients with the NRTI-resistance mutation A62V.
Discussion: Although A62V alone does not reduce NRTI susceptibility, it is an accessory utation that frequently co-occurs with K65R and PMID: 25141905
2014
Journal of the International AIDS Society
Introduction: Q151M is usually accompanied by the mutations A62V, V75I, F77L and F116Y.
2014 Update of the drug resistance mutations in HIV-1.
Discussion: Q151M is the most important mutation in the complex (ie, the other mutations in the complex [A62V, V75I, F77L, and F116Y] in isolation may not reflect multidrug resistance).
Emergence of drug resistance in human immunodeficiency virus type 1 infected patients from pune, India, at the end of 12 months of first line antiretroviral therapy initiation.
Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, M46I/L, I47V/A, I50V, Q58E, A71V, G73S, V82A/F/T, I84V, L89V,L90M; NRTIs resistance mutations are M41L, A62V, PMID: 24358257
2013
PloS one
Result: As summarized in Table 2, all resistant mutations were found as sole mutation, one with A62V, one with D67E and six cases of intermediates at codon 215 (one with T215D, one with T215E, two cases of T215L and two cases of T215S), one with N88D and 14 cases of M46I mutation were detected by conventional bulk sequencing analysis, yielding a drug resistance mutation prevalence of 15.4% (23/149 cases) (Table 2).
Result: The identified A62V, D67E, T215E, T215S and N88D mutations detected by bulk sequencing were not targeted by AS-PCR, and th
Increasing trends in primary NNRTI resistance among newly HIV-1-diagnosed individuals in Buenos Aires, Argentina.
PMID: 24093951
2013
Journal of the International AIDS Society
Method: Sequences were analyzed to identify mutations associated with reduced susceptibility to protease and RT inhibitors, as reported by the International AIDS Society-USA in 2010: RT-M41L, A62V, K65R, D67N, 69 insert, K70R, L74V,V75I, F77L, L100I, K101P, K103N, V106A, V106M, V108I, Y115F, F116Y,
HIV mutation literature information.
PMID: 
2015
PloS one
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