Transmitted drug resistance and phylogenetic relationships among acute and early HIV-1-infected individuals in New York City.
PMID: 22592583
2012
Journal of acquired immune deficiency syndromes (1999)
4Method: ARV resistance was defined by mutations at the following positions: M41L, A62V, K65R, D67N, T69ins, K70R, L74VI, Y115F, Result: D67N(P=0.03), K70R(P=0.06), M184V(P=0.11), L210W(P=0.11), and K219Q(P=0.02) decreased during the study period.
Result: One clustered pair had M46L, another had T215D, and a third had K103N, D67N and K219Q.
Prevalence of Drug Resistance and Associated Mutations in a Population of HIV-1(+) Puerto Ricans: 2006-2010.
Result: Statistically significant differences between men and women were observed for K70R (P = 0.04) and K219Q (P = 0.03) in 2006, K103N (P = 0.02) in 2007, K219E (P = 0.03) in 2009 (data not shown), and V118I (P = 0.03) in 2010.
Assessing subtypes and drug resistance mutations among HIV-1 infected children who failed antiretroviral therapy in Kelantan, Malaysia.
PMID: 22729198
2012
The Brazilian journal of infectious diseases
Abstract: The most prevalent RT mutations were T215F/V/Y (66.7%), D67G/N (55.6%), K219Q/E/R (44.4%), M184V/I (38.9%), K70R/E (27.8%) and M41L (27.8%), associated with nucleoside reverse transcriptase inhibitors (NRTI) resistance; and K103N (55.6%), G190A (33.3%), and K101P/E/H (27.8%) associated with non-nucleoside reverse transcriptase inhibitors (NNRTI) resistance.
Connection domain mutations during antiretroviral treatment failure in Mali: frequencies and impact on reverse transcriptase inhibitor activity.
PMID: 22828721
2012
Journal of acquired immune deficiency syndromes (1999)
Method: Thymidine analogue mutations (TAMs) were defined as M41L, D67N, K70R, L210W, T215F/Y, K219E/Q.
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Abstract: BACKGROUND: Thymidine analogue resistance mutations (TAMs) selected under treatment with nucleoside analogues generate two distinct genotypic profiles in the HIV-1 reverse transcriptase (RT): (i) TAM1: M41L, L210W and T215Y, and (ii) TAM2: D67N, K70R and K219E/Q, and sometimes T215F.
Result: Higher levels of significance were also detected for other pairs of TAMs, such as K70R and K219Q, D67N and K70R, and T215F and K219Q.
Result: Interestingly, <
HIV-1 drug resistance genotyping from antiretroviral therapy (ART) naive and first-line treatment failures in Djiboutian patients.
Discussion: Accumulation of the other mutations observed included thymidine associated mutations (including M41L, D67N, K70R, L210W, T215Y/F, K219Q) results in increasing resistance to AZT, Tenofovir, D4T, Abacavir, and DDI .
Differential in vitro kinetics of drug resistance mutation acquisition in HIV-1 RT of subtypes B and C.
Introduction: Two distinct TAM resistance pathways can be observed: TAM-1 (M41L, T210W and T215Y) and TAM-2 (D67N, K70R, T215F and K219Q).
Virological failure rates and HIV-1 drug resistance patterns in patients on first-line antiretroviral treatment in semirural and rural Gabon.
PMID: 23199801
2012
Journal of the International AIDS Society
Result: TAM-2 mutations included K219Q/E/R (n=4), D67N/G (n=4), and K70R (n=3).
Figure: M41L, L210W, and T215Y mutations are indicative of the TAM-1 pathway; D67N/G, K70R, T215F, and K219Q/E/R mutations are indicative of the TAM-2 pathway.
Low prevalence of transmitted K65R and other tenofovir resistance mutations across different HIV-1 subtypes: implications for pre-exposure prophylaxis.
PMID: 23305651
2012
Journal of the International AIDS Society
Method: Tenofovir-associated resistance mutations included K65R, T69 insertion, K70E and >=3 thymidine-analogue mutations (TAMs; M41L, D67N, K70R, L210W, T215F/Y, K219Q/E), inclusive of either M41L or L210W.
"K70Q adds high-level tenofovir resistance to ""Q151M complex"" HIV reverse transcriptase through the enhanced discrimination mechanism."
Introduction: Increased excision of NRTIs is imparted by Excision Enhancement Mutations, typically M41L, D67N, K70R, T215Y/F, L210W, and K219E/Q (also known as Thymidine Associated Mutations, or TAMs).