Abstract: Examples are Y318F or W, N348I, A376S and T369I or V.
Abstract: Moreover, those mutations could also modulate RNase H activity not only during DNA strand elongation, but also at the initiation of plus strand DNA synthesis as demonstrated for the N348I mutation.
Abstract: Studies on the effects of N348I and A376S on NNRTI resistance indicate that these changes could affect inhibitor binding by altering the interaction between RT subunits or between the RT and the template-primer.
Subunit-specific mutational analysis of residue N348 in HIV-1 reverse transcriptase.
Result: Accordingly, the mechanisms by which N348I decreases RT RNase H activity and drug susceptibility cannot be inferred from this structure.
Result: Accordingly, we generated by site directed mutagenesis six HIV-1 RT constructs that contained the N348I, N348A, N348Q, N348L, N348E or N348R mutations.
Result: As reported previously, N348I significantly reduced the frequency of a polymerase-independent cleavage event that decreases the RNA/DNA duplex to 10 nucleotides (Figure 4B).
Result: As such, their enzyme preparations may have been contaminated by p66N34
Genotypic resistance at viral rebound among patients who received lopinavir/ritonavir-based or efavirenz-based first antiretroviral therapy in South Africa.
PMID: 21694608
2011
Journal of acquired immune deficiency syndromes (1999)
Result: The N348I mutation of the connection domain of RT was detected in two participants; both also had NNRTI mutations.
Discussion: N348I may emerge on NRTI or NNRTI exposure, both of our patients received EFV.
Discussion: The detection of N348I in patients with DRM resistance suggests that sequencing programs that include this portion of RT will be useful in deriving a comprehensive drug resistance evaluation.
Discussion: Two patients in our study developed the connection domain mutation N348I, identified previously as contributing to substantial increase in AZT resistance, including patients with non-subtype B infection.
The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains.
Introduction: N348I confers resistance by reducing RNase H activity which allows more time for the excision or dissociation of the RT inhibitors.
Introduction: Some of these mutations, such as N348I in the connection subdomain, have been reported to have a prevalence of 10-20% in treatment-experienced individuals.
Introduction: The N348I mutation is associated with M184V and TAMs, and increases resistance to NRTIs such as AZT, as well as the NNRTI NVP.
Result: Of note, the N348I mutation was identified in the connection subdomain of all single genomes at 4 months.
Result: Similarly, the coevolved C-terminal region did not contribute to 3TC resistance, including the previously ident
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: N348I or T369I was associated with reduced etravirine susceptibility when present with K101P or K103R/V179D.
Abstract: N348I, E399G, and N348I/T369I were associated with reduced etravirine susceptibility when present with K103N, L100I, or Y181C.
Abstract: Seventeen CDMs were evaluated: L283I, E312Q, G333D, G333E, G335C, G335D, PMID: 21393163
2011
The Journal of antimicrobial chemotherapy
Abstract: Phenotypic analysis of C-terminal mutations showed that N348I, T369V and A371V conferred reduced susceptibility to zidovudine in the context of the TAM-1 and/or TAM-2 pathway, and also conferred dual resistance to nevirapine.
Abstract: RESULTS: Subtype B-infected patient database analysis showed that mutations N348I, A360V/T, T377M and D488E were found to be selected independently of TAMs, whereas mutations R358K, G359S, A371V, A400T, K451R and K512R increased in frequency with the number of TAMs in a dose-dependent fash
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: N348I was probably not identified in our study because efavirenz, not NVP, was the NNRTI used for initial randomized therapy in ACTG A5142 and virologic failure was detected early using a sensitive definition of failure.
Discussion: In this patient, the N348I connection domain mutation was selected by ZDV and/or didanosine therapy and confers resistance to ZDV, didanosine, NVP, EFV, delavirdine, tenofovir and etravirine.
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, N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
PMID: 21282419
2011
Antimicrobial agents and chemotherapy
Abstract: N348I reduced the susceptibility to all NNRTI drugs across subtypes.
Abstract: Interestingly, the N348I and M184V double mutation compensated for the reduced NNRTI drug susceptibility observed in the N348I single mutant and marginally improved viral replicative capacity.
Abstract: The replication capacity of all viruses in a variety of cell lines was impaired by N348I.
Abstract: We investigated the effect of N348I alone and with M184V on nonnucleoside reverse transcriptase inhibitor (NNRTI) drug susceptibility and replicative capacity in B and non-B HIV-1 isolates.
Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
Abstract: Associations between N348I and individual antiretroviral drug exposure were estimated using a matched case-control approach.
Abstract: BACKGROUND: There is conflicting evidence on specific reverse transcriptase inhibitors to which the N348I mutation in the connection domain of HIV type-1 reverse transcriptase confers resistance.
Abstract: CONCLUSIONS: This is the first clinical evidence to suggest that efavirenz might select for N348I in addition to nevirapine, that stavudine might select for N348I in addition to zid
Abstract: Cases were defined as the first resistance test where N348I was detected; for each case, the 10 closest (in calendar time) N348N tests were selected as controls.
Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
Abstract: However, N348I significantly decreases tenofovir susceptibility when combined with thymidine analogue mutations and etravirine susceptibility when combined with Y181C.
Abstract: However, both of these inhibitors are currently infrequently used in developed countries, and the impact of N348I on newer reverse transcriptase inhibitors, such as tenofovir and etravirine, is unknown.
Abstract: In this study, we demonstrate that N348I alone confers no resistance to tenofovir and low-level resistance to etravirine.
Abstract: We previously demonstrated that N348I in HIV-1 reverse transcriptase confers zidovudine and nevirapine resistance.
Introduction: Accordingly, in this study we determined whether
HIV mutation literature information.
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2011
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