Biochemical characterization of a multi-drug resistant HIV-1 subtype AG reverse transcriptase: antagonism of AZT discrimination and excision pathways and sensitivity to RNase H inhibitors.
Abstract: We analyzed a multi-drug resistant (MR) HIV-1 reverse transcriptase (RT), subcloned from a patient-derived subtype CRF02_AG, harboring 45 amino acid exchanges, amongst them four thymidine analog mutations (TAMs) relevant for high-level AZT (azidothymidine) resistance by AZTMP excision (M41L, D67N, T215Y, K219E) as well as four substitutions of the AZTTP discrimination pathway (A62V, V75I, F116Y and Q151M).
Introduction: In HIV-2, AZT discrimination is characterized by the mutations A62V, V75I, F77I, F116Y
Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.
Result: Protease (PR) RAMs detected from this outlier sample were M46I, I47V and I84V, and reverse transcriptase (RT) RAMs were A62V, D67N, K70R, V75I, F116Y,
Discussion: The Q151M complex, consisting of Q151M, A62V, V75I, F77L and F116Y, is associated with resistance to all approved NRTIs except for tenofovir.
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Discussion: In contrast to these earlier reports that identified a limited number of NRTI mutations (T215D, K219Q and D67G, V75A) with a low overall frequency (4.2% and 5.1%, respectively) in newly infected Iranian cases, we detected a variety of NRTI SDRMs (M41L, D67N, K70R, V75M, F116Y, M184V, L210W, T215Y, and K219E) with a higher overall frequency (10%) in chronically infected IDUs in the city of Sanandaj (Table 2).
HIV-1 subtype characteristics of infected persons living in southwestern Greece.
Result: The 22 cases experiencing virologic failure presented with the following DRMs: M46I, F53LY, I54LTV, G73ST, L76V, V82AT, I84V, I185V, N88D, and L90M for PIs; L100I, K103NS, V179F Y181C, G190AS, V106A, K103N, and P225H for NNRTIs; and
In vitro selection of HIV-1 CRF08_BC variants resistant to reverse transcriptase inhibitors.
PMID: 25482475
2015
AIDS research and human retroviruses
Abstract: EFV-associated variations contained two initial mutations (L100I and Y188C) and three other mutations (V106L, F116Y, and A139V).
HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.
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.
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).
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.
HIV mutation literature information.
PMID: 
2016
Nucleic acids research
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