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.

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

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).

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

Result: Additionally, the mutation D67N was incorporated after 77 days (1 microM), when the VL rebounded to original levels before the drug selection.

Result: Interestingly, subtype C followed a different route: it accumulated D67N after 77 days (1 microM) before rebounding and K70R after 84 days (2 microM) during the rebound process.

Result: Nevertheless, the final resistance profile was the same in all replicates: D67D/N, T215Y, F214L (Table 2).

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.

"K70Q adds high-level tenofovir resistance to ""Q151M complex"" HIV reverse transcriptase through the enhanced discrimination mechanism."

PMID: 21249155 2011 PloS one

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).

Discussion: Mutations at position 70 of RT have been known to confer NRTI resistance by two distinct mechanisms: K70R combined with at least two excision enhancing mutations, D67N and T215Y, enhances ATP-mediated excision of AZT and d4T (excision-dependent mechanism).

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