[Screening program on novel drug resistance mutations of subtype B' in human immunodeficiency virus type 1 in China].
PMID: 21569736
2011
Zhonghua liu xing bing xue za zhi
Abstract: RESULTS: Frequencies of 7 mutations at 6 positions, D123E, V292I, K366R, T369A, T369V, A371V and I375V, 2 at DNA polymerase domain and 5 at connection domain of reverse transcriptase (RT) were higher in the treated patients than in the untreated patients.
Connection domain mutations in HIV-1 reverse transcriptase do not impact etravirine susceptibility and virologic responses to etravirine-containing regimens.
PMID: 21464253
2011
Antimicrobial agents and chemotherapy
Abstract: The most prevalent CDMs (>10%) were A371V, E399D, A376S, N348I,
Failure of initial therapy with two nucleosides and efavirenz is not associated with early emergence of mutations in the C-terminus of HIV-1 reverse transcriptase.
PMID: 21350368
2011
Journal of acquired immune deficiency syndromes (1999)
Discussion: These studies have identified a number of mutations in the C-terminus of RT that are more frequent in ART-experienced patients compared to ART-naive including E312Q, G333D/E, G335C/D, N348I, R356K, R358K, A360I/V, A365I, T369I, A371V, A376S and K451R.
Impact of CRF01_AE-specific polymorphic mutations G335D and A371V in the connection subdomain of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) on susceptibility to nucleoside RT inhibitors.
Abstract: Drug susceptibility showed G335D, A371V, or both did not confer resistance by themselves but conferred significant resistance to NRTIs with TAMs, especially in mutants containing G335D, A371V and TAM type 2.
Abstract: In the C-terminal half, G335D (100%), N348I (36.8%), A371V (100%), A376S (5.3%) and A400T (97.4%) were detected, although G335D, A371V and A400T were considered polymorphisms of CRF01_AE.
Abstract: Subsequently, we assessed the impact of CRF01_AE polymorphisms G335D
HIV-1 reverse transcriptase connection domain mutations: dynamics of emergence and implications for success of combination antiretroviral therapy.
Abstract: RESULTS: The connection domain mutations N348I, R356K, R358K, A360V, and A371V were more frequently observed in ART-exposed than ART-naive patients, of which only N348I and A360V were nonpolymorphic (with a prevalence of <1.5% in untreated patients).
Abstract: Several polymorphisms in the C-terminal domain of reverse transcriptase were observed: A371V (in 63.4% of patients), G335D (76.2%), E399D (10.9%) and G333E (1%).
Connection domain mutations in treatment-experienced patients in the OPTIMA trial.
PMID: 20130473
2010
Journal of acquired immune deficiency syndromes (1999)
Abstract: Frequencies of E312Q, Y318F, G333D, G333E, G335C, G335D, N348I, A360I, A360V, V365I, A371V, A376S, and E399G were compared with a treatment-naive population.
Abstract: On univariate analysis, A371V was associated with lack of virologic response, as was having any CD mutation on multivariate analysis.
N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations.
Introduction: In this regard, A371V and Q509L in the connection and RNase H domains, respectively, and mutations located at residues that form part of the RNase H primer grip potentiate resistance to tenofovir in cell culture based assays when combined with TAMs.
Clinical relevance of substitutions in the connection subdomain and RNase H domain of HIV-1 reverse transcriptase from a cohort of antiretroviral treatment-naive patients.
Introduction: also recently reported that the A360V and A371V mutations are frequently observed in AZT-treated patients.
Discussion: A371V was observed in the majority of non-B isolates in our cohort (75%) and the Stanford HIV Drug Resistance Database (96% in CRF01_AE).
Discussion: In our cohort, as well as in the Stanford HIV Drug Resistance Database, we observed a considerable number of treatment-naive clinical samples containing substitutions (E312Q, G333E, G335D, V365I, A371V and A376S) that have been previously associated with AZT resistance.
Mechanism by which a glutamine to leucine substitution at residue 509 in the ribonuclease H domain of HIV-1 reverse transcriptase confers zidovudine resistance.
Introduction: By comparison, A371V in combination with the same TAMs did not augment AZT resistance, although high-level AZT resistance was observed with viruses containing D67N, K70R, T215F, A371V, and Q509L.
Introduction: This study identified two novel mutations in the connection domain (A371V) and RNase H domain (Q509L) of RT that were selected in combination with D67N, K70R, and T215F.
HIV mutation literature information.
PMID: 
2011
Zhonghua liu xing bing xue za zhi
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