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.
Effect of translocation defective reverse transcriptase inhibitors on the activity of N348I, a connection subdomain drug resistant HIV-1 reverse transcriptase mutant.
PMID: 23273211
2012
Cellular and molecular biology (Noisy-le-Grand, France)
Result: 5 shows that N348I mutant RT has decreased RNase H activity for all substrates used in this assay.
Result: 6B) templates suggesting that resistance mutant N348I does not have any significant effect on the unblocking of EFdA-MP containing primers (RNA vs.
Result: ATP-dependent unblocking of EFdA-MP terminated primers by WT and N348I RTs.
Result: Effect of EFdA-MP on RNase H activity of WT and N348I RTs.
Result: Effect of EFdA-MP on Translocation of WT and N348I mutant of HIV-1 RT.
Result: However, the N348I mutation in the background of AZT resistance mutations D
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 <
Discussion: Mutation N348I was verified by Yap et al at the end of 2007 to result in low resistance to AZT, with its degree of AZT resistance increasing with the number of TAMs.
Discussion: Nikolenko et al reported in 2007 that such mutations as E312Q, G335C/D, N348I, A360I/V, V365I and A376S at the connection domain could confer resistance to AZT to a certain extent.
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 PMID: 22618567
2012
Clinical infectious diseases
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.
[Studying on the prevalence and mutation pattern of N348I which related to the resistance of HIV-1].
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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