Abstract: In this study, we have defined the molecular mechanisms of 3'-azido-ddG resistance by performing in-depth biochemical analyses of HIV-1 RT containing mutations L74V, F77L, V106I, L214F, R277K, and K476N (SGS3).
Abstract: We reported that 3'-azido-2',3'-dideoxyguanosine (3'-azido-ddG) selected for the L74V, F77L, and L214F mutations in the polymerase domain and K476N and V518I mutations in the RNase H domain of HIV-1 reverse transcriptase (RT).
HIV multi-drug resistance at first-line antiretroviral failure and subsequent virological response in Asia.
PMID: 25141905
2014
Journal of the International AIDS Society
Introduction: Q151M is usually accompanied by the mutations A62V, V75I, F77L and F116Y.
The lysine 65 residue in HIV-1 reverse transcriptase function and in nucleoside analog drug resistance.
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 (Q151M/A62V/V75I/F77L/F116Y), of which Q151M is one of the primary mutations to emerge.
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and K219QENR; (ii) the
Increased risk of Q151M and K65R mutations in patients failing stavudine-containing first-line antiretroviral therapy in Cambodia.
Result: In our study, other NRTI-RAMs known to be associated with Q151M-mediated multi-nucleoside resistance including A62V, V75I, F77L, and F116Y, were also significantly more common in patients harboring the Q151M mutation (p<0.001).
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,
From the chemistry of epoxy-sugar nucleosides to the discovery of anti-HIV agent 4'-ethynylstavudine-Festinavir.
Introduction: The K65R mutation confers resistance to tenofovir and some NRTIs and, the Q151M complex (A62V, V75I, F77L, F116Y, and Q151M) confers resistance to most of the clinically approved NRTIs.
Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.
Discussion: Q151M is a primary mutation that in vivo can be co-selected together with a group of secondary mutations (A62V, V75I, F77L and F116Y) that confers a cross-resistance with all NRTIs.
Biochemical, inhibition and inhibitor resistance studies of xenotropic murine leukemia virus-related virus reverse transcriptase.
Discussion: In HIV, decreased binding of AZT is conferred initially in the presence of the primary Q151M mutation, followed by secondary mutations F77L, A62V, V75I and F116Y.
HIV mutation literature information.
PMID: 
2014
Antiviral research
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