Result: Similarly, within NRTI SDRMs, K70ER, V75A, F77L, M184I, T215I, and K219E were only found under the 5% threshold, while D67G and M184V, although present in levels >=5% in some patients, were also mostly present as low-abundance variants <5% (0.8% vs.
HIV-1 Antiretroviral Drug Resistance Mutations in Treatment Naive and Experienced Panamanian Subjects: Impact on National Use of EFV-Based Schemes.
Result: In ARV drug-experienced subjects, TAMs found were T215Y/F (26.8%), K70R (15.2%), M41L (13.7%), K219E/Q (12.2%), D67N (10.9%), and L210W (7.5%) (Fig 1A).
Result: In ARV drug-naive subjects, observed TAMs were T215rev (2.0%), T215F (0.4%), M41L (2.0%), K219EQ (0.4%) and L210W (0.4%) (Fig 1A).
Low Incidence of HIV-1C Acquired Drug Resistance 10 Years after Roll-Out of Antiretroviral Therapy in Ethiopia: A Prospective Cohort Study.
Discussion: Despite the extensive use of thymidine analogues like AZT or D4T in Ethiopia and unlike previous similar studies, TAMs characterized by the mutations M41L, L210W, T215Y (TAM-path 1) and D67N, K70R, T215F, K219Q/E (TAM-path 2) were lacking in the current study indicating a recent period of virological failure.
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/
Assessing transmissibility of HIV-1 drug resistance mutations from treated and from drug-naive individuals.
Discussion: We show here that D30N, N88D/S and L90 M also have high transmissibility and that other SDRMs have higher (M41L, T215Rev and K219E/N/Q/R for NRTIs and K101E/P for the NNRTIs) or lower transmissibility (K70E/R, L74I/V, and T215Y/F for NRTIs; Y181C/I/V for NNRTIs and I84 V and I54A/L/M/S/T/V for protease inhibit
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).
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Result: The 22 cases experiencing virologic failure presented with the following DRMs: M46I, F53LY, I54LTV, G73ST, L76V, V82AT, I84V, I185V, N88D, and L90M for PIs; L100I, K103NS, V179F Y181C, G190AS, V106A, K103N, and P225H for NNRTIs; and
Trends on epidemiological, virological, and clinical features among newly diagnosed HIV-1 persons in Northwest Spain over the last 10 years.
Abstract: The most prevalent TDR mutations were: T215 revertants (1.5%), K219QENR (1.2%), for NRTIs; K103N (1.9%), for NNRTIs; L90M (0.3%), for PIs.
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.
HIV mutation literature information.
PMID: 
2016
PloS one
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