Discussion: In contrast to these earlier reports that identified a limited number of NRTI mutations (T215D, K219Q and D67G, V75A) with a low overall frequency (4.2% and 5.1%, respectively) in newly infected Iranian cases, we detected a variety of NRTI SDRMs (M41L, D67N, K70R, V75M, F116Y, M184V, L210W, T215Y, and K219E) with a higher overall frequency (10%) in chronically infected IDUs in the city of Sanandaj (Table 2).
Prediction of drug-resistance using genotypic and docking analysis among anti-retroviral therapy naive and first-line treatment failures in Salem, Tamil Nadu, India.
Abstract: The mutations of I135R/T/V/X, L178 I/M, M184V/I, D67N, K70R, and K103N were the most common among these 23 patients.
Geographic and temporal trends in the molecular epidemiology and genetic mechanisms of transmitted HIV-1 drug resistance: an individual-patient- and sequence-level meta-analysis.
Method: Thymidine-analog mutations (TAMs) were defined as the NRTI SDRMs M41L, D67N/G/E, K70R, L210W, T215Y/F/S/C/D/E/I/V, and K219Q/E/N/R.
Result: Of the 34 NRTI SDRMs, 16 occurred in >=0.1% of the 50,870 viruses from all regions: most commonly M184V, the TAMs (M41L, D67G/N, K70R, L210W, T215F/Y, K219E/Q), the T215 revertants (T215C/D/
AZT resistance alters enzymatic properties and creates an ATP-binding site in SFVmac reverse transcriptase.
Introduction: Amino acid sequence alignments of the polymerase domains of SFVmac and HIV-1 revealed that the SFVmac AZT resistance mutations do not correspond to the ones obtained with highly AZT-resistant HIV-1 RT (M41L, D67N, K70R, T215Y/F and K219Q/E).
Silent mutations at codons 65 and 66 in reverse transcriptase alleviate indel formation and restore fitness in subtype B HIV-1 containing D67N and K70R drug resistance mutations.
Result: Additionally, MNVs emerged in HIVWT during single-cycle infections, with the most frequent MNV located at nucleotide 2744 (RT codon 65) culminating in the emergence of K65K and D67N
Discussion: D67N relative to WT in the presence of ZDV), over multiple cycles of replication in vivo these small fitness gains are likely to be amplified and have clinical implications.
Discussion: Drug resistance mutations change the primary sequence of HIV-1, which can alter the length of homopolymeric stretches of nucleotides, as is the case for D67N in subtype B.
Discussion: Notably, the G to A mutation at 2748 (leading to D67N change) in HIVWT during single-cycle infections is 6-fold higher than the frequency observed in the multiple-cycle infection.
Silent mutations at codons 65 and 66 in reverse transcriptase alleviate indel formation and restore fitness in subtype B HIV-1 containing D67N and K70R drug resistance mutations.
Result: Accordingly, we examined whether the TAMs D67N/K70R increase errors introduced by HIV-1 RT during intracellular RTn that are alleviated by silent mutations K65K and K66K.
Result: Accordingly, we investigated whether HIV-1 harboring K65K or K66K (AAA to AAG change) in the presence of the TAMs, D67N and K70R (HIVTAMK65K and HIVTAMK66K, respectively), potentiated resistance to RT inhibitors.
Result: Based on our previous data showing that K65K and K66K alleviate pausing of recombinant HIV-1 RT during cDNA synthesis of a synthetic RN
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Abstract: The most frequent TDR mutations observed were M41L, D67N/G/E, T215F/Y/I/S/C/D/E/V/N, 219Q/E/N/R, K103N/S, and G190A/S/E in reverse transcriptase, and M46I/L and L90M in protease.
Clinical and virologic follow-up in perinatally HIV-1-infected children and adolescents in Madrid with triple-class antiretroviral drug-resistant viruses.
PMID: 25680310
2015
Clinical microbiology and infection
Abstract: The most common TC-DRM present in >=50% of them were D67NME, T215FVY, M41L and K103N (retrotranscriptase) and L90M (protease).
Mutations in the reverse transcriptase and protease genes of human immunodeficiency virus-1 from antiretroviral naive and treated pediatric patients.
HIV mutation literature information.
PMID: 
2015
PloS one
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