Abstract: N348I may interfere with the initiation of (+)-strand DNA synthesis by reducing polypurine tract (PPT) removal in the presence of nevirapine.
Abstract: The Abstract: The effect of NNRTIs on the RNase H-mediated cleavage of PPT-containing template-primers has been studied with wild-type HIV-1 RT and mutants N348I, T369I, T369V, T376S and N348I/T369I.
Abstract: The enhancing effects of nevirapine and efavirenz were reduced in RTs carrying mutation N348I, and specially N348I/T369I.
In vitro selection of HIV-1 CRF08_BC variants resistant to reverse transcriptase inhibitors.
PMID: 25482475
2015
AIDS research and human retroviruses
Abstract: Initial mutations, in combination with other previously reported substitutions (K20R, D67N, V90I, K101R/E, V106I/A, V108I, F116L, E138R, A139V, V189I, G190A, D218E, E203K, H221Y, F227L, N348I, and T369I) or novel mutations (V8I, S134N, C162Y, L228I
Impact of drug resistance-associated amino acid changes in HIV-1 subtype C on susceptibility to newer nonnucleoside reverse transcriptase inhibitors.
PMID: 25421485
2015
Antimicrobial agents and chemotherapy
Abstract: These included N348I and T369I, amino acid changes in the connection domain that are not generally assessed during resistance testing.
Emergence of drug resistance in human immunodeficiency virus type 1 infected patients from pune, India, at the end of 12 months of first line antiretroviral therapy initiation.
Introduction: Also, the N348I/T369I combination reduces the susceptibility of NNRTIs, and reduces replication capacity of RT.
Introduction: Here, we report an MD study of RT-DNA, RT-DNA-nevirapine(NVP), and N348I/T369I mutant RT-DNA-NVP complexes.
Introduction: The connection mutations N348I or T369I in combination with primary EEMs or NNRTI-resistance mutations enhance NRTI or NNRTI resistance, respectively.
Introduction: Therefore, understanding of (i) the overall struct
The connection domain mutation N348I in HIV-1 reverse transcriptase enhances resistance to etravirine and rilpivirine but restricts the emergence of the E138K resistance mutation by diminishing viral replication capacity.
Abstract: N348I also enhanced levels of resistance conferred by E138K against RPV and ETR by 2.2- and 2.3-fold, respectively.
Abstract: N348I confers resistance to both the NRTI zidovudine (ZDV) and the NNRTI nevirapine (NVP) and was also found to be associated with M184V and to compensate for deficits associated with the latter mutation.
Abstract: In this context, we have investigated the role of a N348I connection domain mutation that is prevalent in treatment-experienced patients.
Abstract: Now, we show that both N348I alone and N348I/M184V can prevent or delay the emergence of E138K
Phenotypic and genotypic analyses to guide selection of reverse transcriptase inhibitors in second-line HIV therapy following extended virological failure in Uganda.
PMID: 24633208
2014
The Journal of antimicrobial chemotherapy
Result: However, in the case of etravirine, K65R, Y115F and the presence of TAMs were associated with increased susceptibility, whilst N348I was associated with decreased susceptibility.
Result: The strength of the univariate effect of the K65R mutation was substantially reduced by the confounding effect of the presence of TAMs or the N348I mutation.
Table: N348I
Discussion: These sensitizing effects outweighed, at group level, an increase in etravirine resistance related to N348I.
Early selection of resistance-associated mutations in HIV-1 RT C-terminal domains across different subtypes: role of the genetic barrier to resistance.
PMID: 24948706
2014
The Journal of antimicrobial chemotherapy
Abstract: N348I was observed in all subtypes, while T369I was only selected in subtype C.
Abstract: RESULTS: N348I, T369I and A360V were found at low prevalence in treatment-naive isolates of all subtypes.
Horizontal gene transfer from human host to HIV-1 reverse transcriptase confers drug resistance and partly compensates for replication deficits.
Abstract: Connection sub-domain mutation, N348I and the M184V active site mutation decreases HIV-1 RT susceptibility to NNRTI, nevirapine (NVP), whereas concurrence of both mutations improves enzyme susceptibility to NVP.
Abstract: Further, for the first time residue interaction network highlighted the structural changes due to occurrence of M184V and N348I mutations which gives a conclusive evidence of these mutations.
Abstract: We showed that the binding of NVP to the NNRTI binding pocket (NNIBP) is drastically distorted in the presence of connection sub-domain mutation, N348I and may further explain the impaired motions of mutant RTs compared to the wild type.
HIV mutation literature information.
PMID: 
2015
Nucleic acids research
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