HIV-1 drug resistance testing is essential for heavily-treated patients switching from first- to second-line regimens in resource-limited settings: evidence from routine clinical practice in Cameroon.
Abstract: Thymidine-analogue mutations (TAMs)-1 [T215FY (46.53%), M41 L (22.77%), L210 W (8.91%)], with cross-resistance to AZT and TDF, were higher compared to TAMs-2 [D67N (21.78%), K70R (19.80%), K219QE (18.81%)].
Result: Of note, TAMs-1 were predominant (T215F/Y: 46.5%; M41 L: 22.8%; L210 W: 8.9%) and associated with higher levels of resistance to both AZT and TDF; as compared to TAMs-2 that had relatively lower prevalence (D67N: 21.8%; K70R: 19.8%; K219Q/E: 18.8%) and were associated preferentially with AZT/D4T-resistance.
Persistence of Human Immunodeficiency Virus-1 Drug Resistance Mutations in Proviral Deoxyribonucleic Acid After Virologic Failure of Efavirenz-Containing Antiretroviral Regimens.
PMID: 30863788
2019
Open forum infectious diseases
Virological outcomes of boosted protease inhibitor-based first-line ART in subjects harbouring thymidine analogue-associated mutations as the sole form of transmitted drug resistance.
PMID: 30544247
2019
The Journal of antimicrobial chemotherapy
Abstract: Most (203 of 269, 75.5%) had singleton TAMs, commonly a revertant of T215Y or T215F (112 of 269, 41.6%).
Introduction: More recently, investigators at Gilead Sciences merged data from a variety of clinical trials and reported that virological responses to 48 weeks of tenofovir-based first-line regimens were not diminished among 205 patients harbouring >=1 TAM, including 76 subjects with revertants of T215Y or T215F (T215rev.
Method: TAMs comprised the RT mutations M41L, D67N/G/E, K70R, L210W, T215Y/F/rev and
Table: T215Y
Drug resistance evolution in patients with human immunodeficiency virus-1 under long-term antiretroviral treatment-failure in Yunnan Province, China.
Abstract: M184 V/I (26.14%), T69S (11.36%), and T215Y/I (10.23%) mutations were the most common in nucleoside reverse transcriptase inhibitors (NRTIs), and K103 N/R/S (21.59%), V179D/E (20.45%) in Non-NRTIs (NNRTIs).
Result: The most common NRTIs mutations were M184 V/I,
Discussion: Two clusters were studied here; TAM-1 (M41 L and T215Y) and TAM-2 (D67N, K70R, and K219Q).
Prevalence and persistence of transmitted drug resistance mutations in the German HIV-1 Seroconverter Study Cohort.
Result: A Kaplan-Meier analysis could be performed for 18 TDRMs (K20T, L23I, K43T, M46I/L/V, I54V, M41L, L74I, M184V, L210W, K219R, T215A/C/D/N/S and T215Y).
Result: The presence of three or more TDRMs was mainly due to the accumulation of Thymidine-Analogue-Mutations (TAMs: M41L, D67N, K70R, L210W, T215F/Y, T215 revertants and K21
Characterization of minority HIV-1 drug resistant variants in the United Kingdom following the verification of a deep sequencing-based HIV-1 genotyping and tropism assay.
Result: Most of these minority drug resistance mutations were detected in the 67 cART-experienced individuals, e.g., the HIV-1 genotype of the following patients consisted of a mixture of majority and minority drug resistance mutations: patient SG79 (PR V11I 99.9%, K20I 99.9%; RT E44D 1.3%, D67N 1.1%, L100I 1.7%, M184V 84.9%, M184I 14.8%, K219Q 2.1%, INT E157Q 99.8%), patient SG86 (RT M184V 99.8%, INT L74M 97.9%, L74I 1.9%, E92Q 86
Resistance profile of children and adolescents infected with HIV-1 in urban areas in Togo.
Result: Thymidine analogue mutations (TAMs) were most frequently seen, with TAM1 mutations (M41L, L210W and T215Y) being most common.
Table: T215Y/F
Distinct Pattern of Thymidine Analogue Mutations with K65R in Patients Failing Tenofovir-Based Antiretroviral Therapy.
PMID: 29084434
2018
AIDS research and human retroviruses
Introduction: Based on significant previous research of DRMs, TAMs have been described to associate into one of two distinct pathways: TAM-1 (M41L, L210W, T215Y) or TAM-2 (D67N, K70R, T215F, K219E/Q).
Introduction: However, in the 31 patients with no K65R present at S2, 6 had intermediate or high-level resistance to AZT: 4 were caused by TAM-2 DRMs, 1 by T215Y, and 1 by Q151M-complex mutations Q151M, A62V, V75I, F77L, F116Y.