Introduction: Among the mutations, N348I and A360V in the connection domain contribute to increasing resistance to zidovudine.
Introduction: The N348I and A360V mutations confer resistance to zidovudine by increasing excision of incorporated zidovudine through RNase H-dependent and independent mechanism.
Introduction: The N348I mutation was reported to be highly correlated with the M184V/I mutation.
Connection subdomain mutations in HIV-1 subtype-C treatment-experienced patients enhance NRTI and NNRTI drug resistance.
Discussion: Stanford University HIV Drug Resistance Database analysis confirmed that three of the identified CN mutations, G335E, N348I and A371V
Discussion: confirmed enhanced ETR resistance for N348I with NNRTI-containing POLs.
Discussion: recently reported that N348I was significantly increased in subtype-C-infected patients failing therapy, and was associated with enhanced resistance to EFV, NVP, ETR and AZT.
Discussion: showed that N348I increases resistance across different subtypes and increases ETV (~2 fold), NVP (~5 fold) and EFV (~3-5 fold) resistance, Furthermore, it was shown that N348I may be selected in the presence of NVP or EFV drug therapy.
Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
PMID: 23273211
2012
Cellular and molecular biology (Noisy-le-Grand, France)
Discussion: Finally, N348I is known to cause resistance to both NRTIs and NNRTIs.
Discussion: Hence, this new class of RT inhibitors should be able to efficiently block viruses that carry clinically relevant mutations, including the new connection domain mutation N348I.
Discussion: This resistance was shown to be caused by N348I, a mutation at the connection subdomain of HIV-1 RT.
Discussion: We report that both EFdA-TP and ENdA-TP are very potent inhibitors of N348I, D67N/Discussion: showed that N348I enhances resistance to AZT through both RNase H-dependent and -independent mechanisms.
Screening for and verification of novel mutations associated with drug resistance in the HIV type 1 subtype B(') in China.
Result: The 9 mutations M41L, D67N, K70R, K103N, Y181C, M184V, T215Y, L283I and N348I resulted in resistance to NRTIs or NNRTIs, but the impact of 7 mutations at 6 positions (D123E, V292I, K366R, T369A, T369V, A371V and I375V) on antiviral drug response was unknown.
Discussion: Mutation N348I was verified by Yap et al at t
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Introduction: N348I or A360V) or its affinity for short RNA/DNA duplexes (e.g.
Introduction: Examples are E312Q, G335C/D, N348I, A360I/V, V365I and A376S in the HIV-1 RT connection subdomain, and Q509L, H539N and D549N in the RNase H domain.
Discussion: In combination with TAMs, N348I and A360V decreased the efficiency of RNase H cleavage and increased excision of AZT in the presence of ATP.
Discussion: Thus, mutations such as N348I,
Connection domain mutations during antiretroviral treatment failure in Mali: frequencies and impact on reverse transcriptase inhibitor activity.
PMID: 22828721
2012
Journal of acquired immune deficiency syndromes (1999)
Abstract: Detected CD mutations were G335D (82.3%), A371V (69.8%), E399D (9.4%), N348I (5.2%), V365I (4.2), Y318F (2.1%), G333E (2.1%), and A360V (2.1%).
Discussion: Also in contrast to our results, studies with approximately 90% B subtype HIV-1 representation reported that N348I and A376S conferred varying degrees of nevirapine resistance, and that E399D conferred resistance to etravirine.
Discussion: Each of the other identified CD mutations (E399D, N348I, V365I, 318F,
Drug resistance mutations in HIV pol sequences from Argentinean patients under antiretroviral treatment: subtype, gender, and age issues.
PMID: 21936717
2012
AIDS research and human retroviruses
Abstract: The most common DRMs were L10I, I54V, L90M, V82A, A71V, L10V, M46I, M184V, M41L, T215Y, D67N, L210W, K70R, N348I, V118I, K103N, Y181C, G190A, K101E, V108I, L100I, V90I, K101Q, and N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
Abstract: N348I emerged at the same time, or after, M184V.
Abstract: N348I in the
Abstract: N348I in the context of polymerase domain mutations reduced susceptibility to NVP (8.9-13-fold), EFV (4-56-fold), etravirine (ETV; 1.9-4.7-fold) and decreased hypersusceptibility to zidovudine (AZT; 1.4-2.2-fold).
Abstract: Additional studies are warranted to characterize the effects of N348I on virologic response to second- and third-line regimens in resource-limited settings where subtype C predominates.
Abstract: CONCLUSIONS: N348I emerges frequently with virologic failure of first-line ART in subtype C HIV-1 infection and reduces susceptibility to NVP, EFV, ETV, and AZT.
Zidovudine (AZT) monotherapy selects for the A360V mutation in the connection domain of HIV-1 reverse transcriptase.
Introduction: For example, the G333D/E, G335C, N348I,
Result: A similar phenotype has been proposed for the A360V mutation; however, the biochemical analyses reported used RTs that also contained N348I.
Result: Previous biochemical studies demonstrated that the N348I and Q509L mutations in HIV-1 RT indirectly increase AZT resistance by decreasing the frequency of secondary RNase H cleavages that reduce the RNA/DNA duplex length of the T/P and diminish the efficiency of AZT-MP excision.
Result: The N348I and Q509L mutations were not detected in any of the 23 on-treatment samples.
Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.
PMID: 22340881
2011
Zhonghua liu xing bing xue za zhi
Abstract: 1233 sequences were then submitted to the HIV-1 drug resistance database of the Stanford University to analyze the prevalence and the emergence pattern of N348I.
Abstract: N348I always emerged, and combined with others mutations among patients of ART, whose frequencies were: 85.0% in combination with thymidine analog mutations (TAMs) and 52.5% with M184V/I, respectively.
Abstract: CONCLUSION: N348I was somehow prevalent in the therapy-failure patients when using the first-line antiretroviral drugs, and it emerged as unique patterns.
Abstract: OBJECTIVE: To elucidate the prevalence and the mutation pattern of N348I that related to the resistance seen in the AIDS patients, in China.
HIV mutation literature information.
PMID: 
2013
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