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
Increasing proportions of HIV-1 non-B subtypes and of NNRTI resistance between 2013 and 2016 in Germany: Results from the national molecular surveillance of new HIV-diagnoses.
Discussion: Large transmission networks of German MSM were observed for the most frequently transmitted NRTI mutation T215S (revertant of T215Y/F), and the PI resistance mutations M46I and V82L.
Resistance profile of children and adolescents infected with HIV-1 in urban areas in Togo.
Discussion: Molecular marker mutations in more than 50% of treatment failure patients were M184V, T215A/Y/F, D67N/G, and M41L.
Discussion: Molecular markers of TAMs, M184V (100%), T215A/Y/F (88.2%), D67N/G (76.5%), and M41L (58.8%), were found in more than 50% of treatment failure patients.
Discussion: There are two clusters of TAMs; cluster 1 includes substitutions of M41L, L210W and T215Y, while cluster 2 of D67N, K70R, T125F and
Risk factors and outcomes for the Q151M and T69 insertion HIV-1 resistance mutations in historic UK data.
Result: Thymidine analogue mutations (TAMs) were most frequently seen, with TAM1 mutations (M41L, L210W and T215Y) being most common.
Table: T215Y/F
Impact of Antiretroviral Regimens on Cerebrospinal Fluid Viral Escape in a Prospective Multicohort Study of Antiretroviral Therapy-Experienced Human Immunodeficiency Virus-1-Infected Adults in the United States.
Result: Given the high frequency of M184V/I detected in all samples (28%, 56/197), these mutations were combined with thymidine-analog mutations (TAMs; ie, M41L, L210W, T215Y, D67N, K70R, T215F, K219Q/E) for analysis.
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.