literature

HIV mutation literature information.

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.

Analysis of the Zidovudine Resistance Mutations T215Y, M41L, and L210W in HIV-1 Reverse Transcriptase.

PMID: 22889300 2012 Retrovirology

Introduction: However, combinations of M41L, D67N, K70R, L210W, T215F/Y and K219E/Q increase ATP-mediated excision of chain-terminating NRTIs (reviewed in ref.).

Introduction: Sequence analysis of HIV-1 isolates from patients receiving long-term therapy with AZT and/or d4T revealed that thymidine analogue resistance mutations (TAMs) acting through the excision mechanism associated in two different clusters: TAM1 (M41L, L210W and T215Y) and TAM2 (D67N, K70R, K219E/Q, and sometimes T215F).

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.

PMID: 22889300 2012 Retrovirology

Result: M41L, D67N,

Result: Amino acid substitutions D67N, L74I, K223E and L228H associate with the TAM2 cluster, while V118I, V179I, M184V and R284K are linked to cluster (2) formed by mutations of the TAM1 pathway.

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.

HIV-1 drug resistance genotyping from antiretroviral therapy (ART) naive and first-line treatment failures in Djiboutian patients.

PMID: 23044036 2012 Diagnostic pathology

Result: The NRTI-associated mutations were D67N (2 strains), T69N (1), M184V (6), L210W (2), T215Y (2).

Table: D67N

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.

PMID: 23056372 2012 PloS one

Discussion:

Discussion: Although some researchers characterize D67N as a TAM-2 pathway mutation, this change has also been found in a TAM-1 background, in agreement with our data.

Discussion: Furthermore, an additional mutation, D67N, was incorporated when the VL rebounded to original levels comparable to those before the onset of drug selection (figure 1B).

Screening for and verification of novel mutations associated with drug resistance in the HIV type 1 subtype B(') in China.

PMID: 23144802 2012 PloS one

Result: The 9 mutations M41L, D67N, K70R, K103N, Y181C, M184V, T215Y, L283I and N348I resulted in resistance to NRTIs or NNRTIs, but the impact of 7 mutations at 6 positions (D123E, V292I, K366R, T369A, T369V, A371V and I375V) on antiviral drug response was unknown.

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.

Monitoring HIV viral load in resource limited settings: still a matter of debate?

PMID: 23236346 2012 PloS one

Result: Among patients carrying RAMs, 12/15 (80.0%) harboured RAMs associated to thymidine analogues (TAMs) (M41L, D67N, K70R, V75I, L210W, T215F/Y) (Table 3).

Result: One patient carried Q151M mutation, associated with M41L, D67N, T215F and M184V, conferring pan-nucleoside resistance, except to tenofovir.

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%),

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)

Result: N348I, D67N/K70R/L210Q/T215F and D67N/K70R/L210Q/T215F/N348I RTs were inhibited by EFdA-TP and ENdA-TP with similar efficiency compared to the WT enzyme.

Result: However, the N348I mutation in the background of AZT resistance mutations D67N, K70R, L210Q and T215F showed a 2-fold increase in unblocking EFdA-MP containing primers both with DNA and RNA templates.

Result: The inhibition of WT,

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.

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