HIV mutation literature information.


  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)
Abstract: In this study we tested EFdA-triphosphate (TP) together with a related compound, ENdA-TP (4'-ethynyl-2-amino-2'-deoxdyadenosine triphosphate) against HIV-1 RTs that carry clinically relevant drug resistance mutations: N348I, D67N/K70R/L210Q/T215F, D67N/K70R/L210Q/T215F/N348I, and A62V/V5I/F77L/F116Y/Q151M.
Introduction: In this study we determine the ability of TDRTIs to block reverse transcription


  "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 Q151M mutation together with a cluster of four additional mutations (A62V/V75I/F77L/F116Y).
Discussion: Also,


  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: Population sequencing of the entire reverse transcriptase (RT) gene identified L74V, F77L, and L214F mutations in the polymerase domain and K476N and V518I mutations in the RNase H domain.


  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
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.


  Low-abundance HIV species and their impact on mutational profiles in patients with virological failure on once-daily abacavir/lamivudine/zidovudine and tenofovir.
 PMID: 20008905       2010       The Journal of antimicrobial chemotherapy
Result: Mutations detected by CG at baseline that could have impacted response to one or more study drugs included mutations at T215, K70E, D67G, M184V and the multi-NRTI Q151M-associated mutations A62V and F77L.
Result: Seven of the VF subjects at baseline had resistance mutation-containing low-abundance viral species (including one of more of the following: A62V, F77L, K70E, T215A, T215S, D67G, M184V or K219Q) with the potential to impact response to one or more st


  Proteochemometric modeling of the susceptibility of mutated variants of the HIV-1 virus to reverse transcriptase inhibitors.
 PMID: 21179544       2010       PloS one
Result: Analyzing the PLS regression equation further reveals that the over-predicted FDS for isolate 75739 versus AZT (shown as the AZT-75739 encircled point in bottom right corner of Figure 1) arises mainly due to an F77L mutation.


  The K65R mutation in HIV-1 reverse transcriptase: genetic barriers, resistance profile and clinical implications.
 PMID: 20190870       2009       HIV therapy
Introduction: In addition, AZT and d4T may also select for the more rarely observed Q151M nucleoside analog mutational (NAM) pathway (Q151M, A62V, V75I, F77L and F116Y), which confers broad-spectra NRTI resistance.
Introduction: The K65R pathway may be associated with the NAM pathway, which is associated with the Q151M, A62V, V75I, F77L and F116Y mutations.


  Clinical and genotypic findings in HIV-infected patients with the K65R mutation failing first-line antiretroviral therapy in Nigeria.
 PMID: 19644383       2009       Journal of acquired immune deficiency syndromes (1999)
Result: Among the 13 patients on non-TDF ART, the following NRTI mutations were observed in association with the K65R mutation: Q151M, F77L, F116Y, V75I, M184V, K219R, T69del and S68G.


  The prevalence of resistance-associated mutations to protease and reverse transcriptase inhibitors in treatment-naive (HIV1)-infected individuals in Casablanca, Morocco.
 PMID: 19759509       2009       Journal of infection in developing countries
Abstract: Only one patient of 70 (1.4%) carried the F77L mutation that is associated with NRTIs resistance.


  Antiretroviral drug resistance in HIV-2: three amino acid changes are sufficient for classwide nucleoside analogue resistance.
 PMID: 19358668       2009       The Journal of infectious diseases
Result: 3.1 +- 0.3 mumol/L, for Q151M and Q151M+3, respectively), indicating that A62V, F77L, and Y116F do not enhance AZT resistance in HIV-2.
Result: Although A62V, F77L, and Y116F increase the level of Q151M-mediated AZT resistance in HIV-1, the Q151M and Q151M+3 variants of HIV-2ROD exhibited comparable sensitivity to the drug (mean EC50 [+-SD], 5.2 +- 2.3 vs.
Result: Surprisingly, the dose-response profile of Q151M HIV-2ROD was comparable to that of the highly resistant Q151M/A62V/



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