Failure of initial therapy with two nucleosides and efavirenz is not associated with early emergence of mutations in the C-terminus of HIV-1 reverse transcriptase.
PMID: 21350368
2011
Journal of acquired immune deficiency syndromes (1999)
Discussion: Other known polymerase domain mutations were not significantly associated with failure although, there were possible trends for K65R (p=0.13) and V106I/M (p=0.13).
Predicted susceptibility of etravirine in HIV patients experiencing virological failure secondary to non-nucleoside reverse transcriptase inhibitor resistance in Argentina.
PMID: 21592625
2011
Enfermedades infecciosas y microbiologia clinica
Abstract: ETR-RAMs were defined as V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S, and M230L, and were analyzed according to the weighted mutation score to predict susceptibility (Vingerhoets 2008).
HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
Abstract: We also showed that EFV stimulates K101E+Y188L and K101E+V106I virus, but not K101E+L100I, K101E+K103N, K101E+Y181C, or K101E+G190A virus, suggesting that the stimulation is mutation specific.
1-[2-(2-Benzoyl- and 2-benzylphenoxy)ethyl]uracils as potent anti-HIV-1 agents.
Result: Next, in order to more fully understand the activity of the benzophenones against drug-resistant HIV strains as well as to verify the reasons for the poor levels of activity of the compounds against the K103N/Y181C RT double mutant virus, a panel of RT's bearing one or two of the most clinically significant mutations (L100I, K103N, V106I, Y181C, Y188L, G190A, and K103N/Y181C) conferring resistance of the virus to NNRTIs was constructed.
TMC278, a next-generation nonnucleoside reverse transcriptase inhibitor (NNRTI), active against wild-type and NNRTI-resistant HIV-1.
PMID: 19933797
2010
Antimicrobial agents and chemotherapy
Abstract: NNRTI RAMs emerging in HIV-1 under selective pressure from TMC278 included combinations of V90I, L100I, K101E, V106A/I, V108I, E138G/K/Q/R, V179F/I, Y181C/I, V189I, G190E, H221Y, F227C, and M230I/L.
N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations.
Introduction: Since the presence of three or more NNRTI mutations V90I, A98G, L100I, K101E/P, V106I, V179D/F, Y181C/I/V and G190A/S results in no response to etravirine treatment, the presence of two of these NNRTI mutations and N348I at baseline may also reduce etravirine efficacy in vivo.
HIV-1 primary and secondary antiretroviral drug resistance and genetic diversity among pregnant women from central Brazil.
Abstract: Naive patients had accessory mutations in the PR gene [A71T (1/6), L10V (2/6), L10I (3/6)] and in the RT gene [V118I (2/6), V179D (1/6), V106I (1/6), K101Q (1/6), H221Y (1/6)].
Baseline-transmitted V106V/I/M non-nucleoside reverse transcriptase inhibitor resistance in HIV-1 subtype B infection.
PMID: 20124001
2010
Antimicrobial agents and chemotherapy
Abstract: Analysis of recombinant HIV-1 clones showed that the combination of V106I and V179D conferred significant resistance to EFV and nevirapine (NVP) but not to ETV.
Abstract: Following its introduction, two naturally occurring mutations in HIV-1 RT, V106I and V179D, were listed as ETV resistance-associated mutations.
Abstract: Interestingly, V179D emerged in one of three selection experiments from HIV-1(V106I) and V106I emerged in two of three experiments from HIV-1(V179D).
Abstract: Structural analysis indicated that ETV can overcome the repulsive interactions caused by the combination of V106I and
Efficacy and safety of 1-month postpartum zidovudine-didanosine to prevent HIV-resistance mutations after intrapartum single-dose nevirapine.
HIV mutation literature information.
PMID: 
2011
Journal of acquired immune deficiency syndromes (1999)
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