HIV mutation literature information.


  "K70Q adds high-level tenofovir resistance to ""Q151M complex"" HIV reverse transcriptase through the enhanced discrimination mechanism."
 PMID: 21249155       2011       PloS one
1Abstract: HIV-1 carrying the ""Q151M complex"" reverse transcriptase (RT) mutations (A62V/V75I/F77L/F116Y/Q151M, or Q151Mc) is resistant to many FDA-approved nucleoside RT inhibitors (NRTIs), but has been considered susceptible to tenofovir disoproxil fumarate (TFV-DF or TDF)."
Introduction: This RT contains the
Discussion: Also, Q151M and associated mutations A62V, V75I, and F77L are likely to modify the hydrophobic core of the fingers.


  Thermostable HIV-1 group O reverse transcriptase variants with the same fidelity as murine leukaemia virus reverse transcriptase.
 PMID: 21446917       2011       The Biochemical journal
Abstract: K65R, K65R/V75I and <
Abstract: At temperatures above 52C, K65R and K65R/V75I retained similar levels of DNA polymerase activity to the wild-type HIV-1 group O RT, but were more efficient than HIV-1 group M subtype B and MLV RTs.
Abstract: Forward-mutation assays demonstrated that mutant RTs K65R, R78A and K65R/V75I showed >9-fold increased accuracy in comparison with the wild-type enzyme and were approximately two times more faithful than the MLV RT.


  Drug resistance mutations in patients infected with HIV-2 living in Spain.
 PMID: 21558334       2011       The Journal of antimicrobial chemotherapy
Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I


  The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains.
 PMID: 21569325       2011       Retrovirology
Abstract: The emergence of Q151M MDR occurred in the order A62V, V75I, and finally Q151M on the same genome at 4, 17 and 37 months after initiation of therapy, respectively.
Introduction: The Q151M MDR complex is composed of the Q151M mutation, which is normally the first to appear, followed by at least two of the following four mutations: A62V, V75I, F77L and F116Y.
Result: Genetic linkage analysis of the single genomes at 4, 17 and 37 months showed that the patient acquired the Q151M MDR mutations in the order: A62V, V75I and finall


  The base component of 3'-azido-2',3'-dideoxynucleosides influences resistance mutations selected in HIV-1 reverse transcriptase.
 PMID: 21646480       2011       Antimicrobial agents and chemotherapy
Abstract: In contrast to 3'-azido-ddG, 3'-azido-ddC selected for the V75I mutation in HIV-1 RT that conferred 5.9-fold resistance, compared to the wild-type virus.


  Drug resistance patterns and virus re-suppression among HIV-1 subtype C infected patients receiving non-nucleoside reverse transcriptase inhibitors in South Africa.
 PMID: 21927716       2011       Journal of AIDS & clinical research
Result: Overall, 8/38 (21%) had one or more TAMs, three had A62V or V75I and only one patient had K65R.


  Resistance patterns selected by nevirapine vs. efavirenz in HIV-infected patients failing first-line antiretroviral treatment: a bayesian analysis.
 PMID: 22132100       2011       PloS one
Result: TDF was also associated with lower risk of mutation M184V (PP[OR<1] = 99%) and with less significance, of mutation V75I (PP[OR<1] = 89%).


  Impact of HIV-1 Integrase L74F and V75I Mutations in a Clinical Isolate on Resistance to Second-Generation Integrase Strand Transfer Inhibitors.
 PMID: 20009920       2010       AIDS (London, England)
Abstract: We show that the V75I variant has decreased sensitivity to some nucleoside analogs but an increased sensitivity to zidovudine, results that may guide selection of highly active antiretroviral therapy regimens in patients harboring this variant.


  K65R and K65A substitutions in HIV-1 reverse transcriptase enhance polymerase fidelity by decreasing both dNTP misinsertion and mispaired primer extension efficiencies.
 PMID: 20538005       2010       Journal of molecular biology
Discussion: In RTs containing V75I, a secondary mutation associated with mutations conferring resistance to both ddNTPs and NNRTIs, there is an increase in incorporation fidelity and, to a greater degree, a decrease in efficiency of mismatch extension.
Discussion: The mechanism through which V75I acts is less clear, as the residue does not interact directly with the incoming dNTP, but does interact with the template overhang.


  Drug resistance is widespread among children who receive long-term antiretroviral treatment at a rural Tanzanian hospital.
 PMID: 20576637       2010       The Journal of antimicrobial chemotherapy
Table: V75I



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