literature

HIV mutation literature information.

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.

Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.

PMID: 20160634 2010 AIDS (London, England)

Abstract: CONCLUSION: The acquisition of N348I in HIV-1 reverse transcriptase - which can occur early in therapy, oftentimes before TAMs - may provide a simple genetic pathway that allows the virus to select both TAMs and mutations that are antagonistic toward TAMs.

Abstract: DESIGN AND METHODS: The ZDV monophosphate and ribonuclease H activities of recombinant-purified HIV-1 reverse transcriptase-containing combinations of K70R, N348I and Y181C, L74V or M184V were assessed using standard biochemical and antiviral assays.

Abstract: However, the N348I mutation compensated for this antagonism on RNA/DNA template/primers by significantly decreasing the frequency of secondar

Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.

PMID: 20170373 2010 The Journal of infectious diseases

Abstract: BACKGROUND: The connection domain mutation N348I confers resistance to zidovudine (AZT) and is associated with the lamivudine (3TC) mutation M184V.

Abstract: Biochemical data show that N348I can partially compensate for the diminution in processive DNA synthesis and the reduction in AZT excision associated with M184V.

Abstract: CONCLUSION: In vivo selection of N348I is driven by AZT and is further facilitated when 3TC is coadministered.

Combinations of mutations in the connection domain of human immunodeficiency virus type 1 reverse transcriptase: assessing the impact on nucleoside and nonnucleoside reverse transcriptase inhibitor resistance.

PMID: 20194692 2010 Antimicrobial agents and chemotherapy

Abstract: Furthermore, the effect of N348I on NRTI and NNRTI resistance was confirmed.

Abstract: HIV-1 with either N348I or T369I/V demonstrated reduced susceptibility to nevirapine (NVP), efavirenz (EFV), delaviridine (DLV), and zidovudine (ZDV) compared to wild-type HIV-1.

Abstract: However, HIV-1 with T369I and N348I demonstrated 10- to 60-fold resistance to these same drugs.

Drug-resistant mutation patterns in CRF01_AE cases that failed d4T+3TC+nevirapine fixed-dosed, combination treatment: Follow-up study from the Lampang cohort.

PMID: 20382184 2010 Antiviral research

Abstract: CRF01_AE-specific polymorphisms were found in 19 residues, and GPOvir-failure cases had significantly higher frequency of N348I, E399D, P537S, and I542M.

Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.

PMID: 20530477 2010 The Journal of biological chemistry

Abstract: N348I has been associated with resistance to the non-nucleoside RT inhibitor (NNRTI), nevirapine; however, a possible mechanism that links changes in RNase H activity to changes in NNRTI susceptibility remains to be established.

Abstract: Here we demonstrate that RNase H-mediated primer removal is indeed more efficient in the presence of NNRTIs; however, the N348I mutant enzyme is able to counteract this effect.

Abstract: The data are in agreement with clinical data, which demonstrate a stronger effect of N348I on susceptibility to nevirapine as compared with efavirenz.

HIV-1 reverse transcriptase connection domain mutations: dynamics of emergence and implications for success of combination antiretroviral therapy.

PMID: 20666602 2010 Clinical infectious diseases

Abstract: N348I correlated with M184V and predominantly occurred in patients receiving lamivudine and zidovudine concomitantly.

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).

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.

PMID: 20713171 2010 Microbes and infection

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.

Compensatory role of double mutation N348I/M184V on nevirapine binding landscape: insight from molecular dynamics simulation.

PMID: 20876531 2010 The Journal of biological chemistry

Abstract: In conclusion, connection subdomain mutation N348I decreases catalytic efficiency and causes in vitro resistance to NVP by decreasing inhibitor binding.

Abstract: Mutation in p66 alone (p66(N348I)/p51(WT)) caused NVP resistance without significantly affecting RNase H activity, whereas mutation in p51 caused NVP resistance and impaired RNase H, demonstrating that NVP resistance may occur independently from defects in RNase H function.

Abstract: Surprisingly, mutation in either subunit decreased catalytic rates (k(pol)) of p66(N348I)/p51(N348I), p66(N348I)/p51(WT), and p66(WT)/p51(N348I) without significantly affecting affinity for deoxynucleotide substrate (K(d)(-dNTP)).

Mutations in the thumb-connection and RNase H domain of HIV type-1 reverse transcriptase of antiretroviral treatment-experienced patients.

PMID: 19430098 2009 Antiviral therapy

Abstract: CONCLUSIONS: RT mutations at three positions outside of the polymerase region were associated with antiretroviral therapy: R284K, N348I and K451R.

Abstract: In treatment-experienced patients, 17.3% had R284K, whereas 24.5% had N348I substitutions.

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