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 HIV mutation literature information.


  Two Coselected Distal Mutations in HIV-1 Reverse Transcriptase (RT) Alter Susceptibility to Nonnucleoside RT Inhibitors and Nucleoside Analogs.
 PMID: 30894467       2019       Journal of virology
Table: A360V


  Biochemical characterization of a multi-drug resistant HIV-1 subtype AG reverse transcriptase: antagonism of AZT discrimination and excision pathways and sensitivity to RNase H inhibitors.
 PMID: 26850643       2016       Nucleic acids research
Result: E312Q, G335C/D, N348I, A360I/V, V365I and A376S) have been identified that significantly contribute to AZT resistance by reducing RNase H activity.


  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: A360V and T369V were selected by RTI treatment in several subtypes.
Abstract: RESULTS: N348I, T369I and A360V were found at low prevalence in treatment-naive isolates of all subtypes.


  From the chemistry of epoxy-sugar nucleosides to the discovery of anti-HIV agent 4'-ethynylstavudine-Festinavir.
 PMID: 23092278       2013       Current pharmaceutical design
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.


  Connection subdomain mutations in HIV-1 subtype-C treatment-experienced patients enhance NRTI and NNRTI drug resistance.
 PMID: 23068886       2013       Virology
Introduction: Associations of these and other CN mutations with drug exposure and TAMs has also been confirmed through other subtype-B-infected patient cohorts and in vitro studies Recently, CN mutation A360V was shown to be selected in subtype-B-infected patients receiving AZT monotherapy.
Introduction: Eight novel mutations, E312Q, G335C/D, N348I, A360I/V, V365I, and A376S, were identified within the CN of RT that significantly contributed to AZT resistance, and these mutations were further found to decrease RNase H activity, leading to decreased susceptibility to AZT.
Introduction: We further analyzed 450 subtype B isolates from the Stanford University HIV Drug Resistance Database and show


  Screening for and verification of novel mutations associated with drug resistance in the HIV type 1 subtype B(') in China.
 PMID: 23144802       2012       PloS one
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.
 PMID: 22889300       2012       Retrovirology
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.


  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)
Discussion: Each of the other identified CD mutations (E399D, N348I, V365I, 318F, G333E, and A360V) was less than 10% prevalent.
Discussion: In another study, N3481, R356K, R358K, A360V and A371V were more frequently detected in ART-exposed compared with ART-naive subtype B patients.
Discussion: In subtype B, CD mutations that have been associated with resistance include E312Q, G333E/D, G335D, N3481, A360I/V, V365I, T369I,


  Zidovudine (AZT) monotherapy selects for the A360V mutation in the connection domain of HIV-1 reverse transcriptase.
 PMID: 22363673       2012       PloS one
Abstract: Biochemical studies revealed that A360V enhances the AZT-monophosphate excision activity of purified RT by significantly decreasing the frequency of secondary RNase H cleavage events that reduce the RNA/DNA duplex length and promote template/primer dissociation.
Abstract: CONCLUSIONS: The A360V mutation in the connection domain of RT was selected in HIV-infected individuals that received AZT monotherapy and contributed to AZT resistance.
Abstract: HIV-1 drug susceptibility assays demonstrated that A360V, either alone or in combination with thymidine analog mutations, decreased AZT susceptibility in recombinant viruses containing participant-derived full-length RT sequences or site-directed mutant


  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: Seventeen CDMs were evaluated: L283I, E312Q, G333D, G333E, G335C, G335D, N348I, A360I, A360T, A360V, V365I, T369I, A371V, A376S, I393L, E399D, and E399G.
Abstract: The presence or number of CDMs did not significantly reduce etravirine susceptibility, although small reductions were seen in samples with G333D, N348I,



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