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
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 K219Q/E/N/R; T215rev comprised any change from T215 other than T215Y and T215F.
Table: T215Y
Drug resistance evolution in patients with human immunodeficiency virus-1 under long-term antiretroviral treatment-failure in Yunnan Province, China.
Result: The most common NRTIs mutations were M184 V/I, T69S, and T215Y/I, with DR rates of 37.7, 16.39, and 14.75%, respectively.
Result: The mutation M184 V/I principally appeared in the first antiviral treatment failure, whereas the T215Y/I mutation was mainly associated with the second and third occasions.
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 pr
Discussion: In contrast, the mean survival times determined for NRTI mutations T215Y/A/N and L74I, which were also found at a lower proportion among the transmitted NRTI mutations, ranged from 1.0 to 1.7 years.
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.
Abstract: Molecular marker mutations, which were found in more than 50% of treatment failure patients, were M184V (100%), T215A/Y/F (88.2%), D67N/G (76.5%), and M41L (58.8%).
Result: The result shows that molecular marker mutations, which were found in more than 50% of treatment failure patients, were M184V (100%), T215A/Y/F (88.2%), D67N/G (76.5%), and M41L (58.8%).
Discussion: Molecu
Discussion: Molecular marker mutations in more than 50% of treatment failure patients were M184V, T215A/Y/F, D67N/G, and M41L.
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.