Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N, T69D/N, L210W, K219Q/E in RT and L10I/V, L63P, A71V/T, V77I in PR)
Clinical significance of HIV reverse-transcriptase inhibitor-resistance mutations.
Abstract: Several large-scale HIV-1 genotypic analyses have revealed that the most prevalent nucleos(t)ide analog RT inhibitor (NRTI)-resistance mutation is M184V/I followed by a series of thymidine analog-associated mutations: M41L, D67N, K70R, L210W, T215Y/F and K219Q/E.
HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
Result: Nineteen samples had major NRTI mutations, specifically K219E/Q (n=8), L74V (n=7), K70E (n=3), D67N (n=2) and L210W (n=1).
High prevalence of HIV-1 drug resistance among patients on first-line antiretroviral treatment in Lome, Togo.
PMID: 21663632
2011
Journal of the International AIDS Society
Result: Two patients had virus mutations indicative of the TAM-1 profile (M41L, L210W, T215S), and two of the TAM-2 profile (D67N, K70R, T215F, K219Q/R/E).
Table: K219Q
Transmission of HIV drug resistance and non-B subtype distribution in the Spanish cohort of antiretroviral treatment naive HIV-infected individuals (CoRIS).
Abstract: The most prevalent resistance mutations were: T215 revertants (3.8%), D67NG (1.3%), K219QENR (1.2%) and M41L (1%), for NRTIs; K103N (3.2%), for NNRTIs; I54VLMSAT, M46I and L90M (0.7%), for PIs.
Transmitted drug resistance in the CFAR network of integrated clinical systems cohort: prevalence and effects on pre-therapy CD4 and viral load.
Abstract: We found that causal effect estimates of mutations M184V/I (-1.7 log10pVL) and D67N/G (-2.1[3 CD4] and 0.4 log10pVL) were compensated by K103N/S and K219Q/E/N/R.
Discussion: Our results give the first evidence that the transmission of
Discussion: Previous studies have also documented compensatory/epistatic interactions of other mutations acting on M184V/I, including K219Q and N384I.
Discussion: Similarly, we have observed several compensatory interactions among mutations that would otherwise mask the actual effects of individual mutations on CD4 or pVL (e.g., D67N/G and K219Q/E).
The glutamine side chain at position 91 on the beta5a-beta5b loop of human immunodeficiency virus type 1 reverse transcriptase is required for stabilizing the dNTP binding pocket.
Result: have reported a concomitant increase in the processivity of the mutant enzyme D76N, K70R, T215F, and K219Q to compensate for the increased pyrophosphorolysis, which they attribute to alterations T215F and K219Q.
Result: have reported such enhanced pyrophosphorolysis in HIV-1 RT due to mutations D76N/K70R in the high-level resistance mutants D76N, K70R,
Drug resistance patterns and virus re-suppression among HIV-1 subtype C infected patients receiving non-nucleoside reverse transcriptase inhibitors in South Africa.
PMID: 21927716
2011
Journal of AIDS & clinical research
Discussion: Among eight patients with TAMs, the most common pathway (seen in 6/8 patients) was TAM-2 related (D67N, K70R, K219Q/R/E); and the rest (2/8) were mixed with the TAM-1 pathway (M41L, L210W, T215Y) extending similar prior Southern African observations.
A structural frame for understanding the role of thymidine analogue resistance mutations in resistance to zidovudine and other nucleoside analogues.
Result: Longer duration of virologic failure was found significantly associated with higher risk of all TAM-2 mutations (D67N, K70R, K219Q/E, T215F) and the
Discussion: Our analysis offers strong evidence that, in contrast to the mutation patterns published for other subtypes, individuals infected with CRF01_AE and experiencing virologic failure while receiving NVP-based HAART favor TAM-2 resistance pathways (K70R, D67N, T215F, K219Q/E) rather than TAM-1 (M41L, L210W, T215Y), whereas those receiving regimens containing EFV appear to select both TAM-2 and TAM-1 pathways (Figures 1B, 2A and 3B).
HIV mutation literature information.
PMID: 
2011
PloS one
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