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 Q151M complex of mutations was defined as Q151M alone or in combination with one or more of the following mutations: A62V, V75I, F77L, and F116Y.
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).
Major groove binding track residues of the connection subdomain of human immunodeficiency virus type 1 reverse transcriptase enhance cDNA synthesis at high temperatures.
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.
Low rates of nucleoside reverse transcriptase inhibitor resistance in a well-monitored cohort in South Africa on antiretroviral therapy.
Introduction: showed that the mutation Val75Ile increased the mismatch extension fidelity 3-fold while showing no apparent effect on misinsertion fidelity.
Differential in vitro kinetics of drug resistance mutation acquisition in HIV-1 RT of subtypes B and C.
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.
Monitoring HIV viral load in resource limited settings: still a matter of debate?
Result: The most frequent TAMs were T215F/Y (11/12, 91.7%), M41L (10/12, 83.3%), L210W (3/12, 27,3%), D67N (3/12, 25.0%), K70R (1/12, 8.3%) and V75I (1/12, 8.3%) (Table 3).
Table: V75I
Effect of translocation defective reverse transcriptase inhibitors on the activity of N348I, a connection subdomain drug resistant HIV-1 reverse transcriptase mutant.
PMID: 23273211
2012
Cellular and molecular biology (Noisy-le-Grand, France)
8Discussion: The A62V/V75I/F77L/F116Y/Q151M set of mutations is known as the ""Q151M"" complex RT, and has been known as a multidrug-resistance mutation, since the latter mutations are known to be involved in resistant variants with reduced susceptibility to dideoxynucleotides and to AZT."
Result: In addition, another mutant HIV-1 RT (A62V/V75I/F77L/F116Y/Q151M) was included in drug susceptibility assays.
Discussion: We report that both EFdA-TP and ENdA-TP are very potent inhibitors of N348I,
Herpes simplex virus type 2 suppressive therapy with acyclovir or valacyclovir does not select for specific HIV-1 resistance in HIV-1/HSV-2 dually infected persons.
PMID: 21148504
2011
The Journal of infectious diseases
Abstract: No V75I cases were detected (95% confidence interval, 0%-2.2%).
Abstract: Recent in vitro studies suggest that acyclovir may directly inhibit HIV-1 replication and can select for a specific HIV-1 reverse transcriptase mutation (V75I) with concomitant loss of an anti-HIV-1 effect.
Introduction: However, in vitro studies have suggested that acyclovir may directly inhibit HIV-1 replication, with acyclovir exposure selecting for a single-base pair mutation in HIV-1 reverse transcriptase (RT) that results in an amino acid substitution at codon 75 (V75I) that confers resistance to the anti-HIV-1 effect of acyclovir.
Introduction: Using a highly-sensitive oligonucleotide ligation assay (OLA), we screened for the V75I mutation in pl
HIV mutation literature information.
PMID: 
2013
PloS one
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