HIV mutation literature information.


  Emergence of HIV-1 drug resistance mutations in mothers on treatment with a history of prophylaxis in Ghana.
 PMID: 30223845       2018       Virology journal
Result: The major DRAMs to PIs seen in the group was I84V; the minor drug resistance mutations seen were A71V, L89 V and M46MV.


  HIV-1 infection among crack cocaine users in a region far from the epicenter of the HIV epidemic in Brazil: Prevalence and molecular characteristics.
 PMID: 30016324       2018       PloS one
Abstract: Five isolates had secondary mutations to protease inhibitors (K20M, L10V, L33I, A71T, A71V).
Result: No major mutation to PI was identified; however, five isolates presented minor PI mutations (K20M: BRGO_CK4, subtype B; A71V: BRGO_CK600, subtype B; L10V: BRGO_CK496, subtype B; A71T and L33I: BRGO_CK311, subtype B; L10V: BRGO_CK117, subtype C).


  Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.
 PMID: 29511083       2018       mBio
Discussion: In addition, A71V is also known as one of the common polymorphisms found in several percent PI-naive patients.
Discussion: In contrast, a set of data compiled for NDA21-976/S003 and NDA21-976/S004 clearly indicates that 10 amino acid substitutions including L10F, V32I, L33F, S37N, M46I, I47V
Discussion: It is interesting that when rHIVL33F/I84V was selected, this clone continued to propagate in the presence of increasing concentrations of DRV, acquired V32I (as examined at week 26) but without acquiring A71V, and became capable of propagating in the presence of 1 microM DRV by 26 weeks of selection.


  HIV drug resistance in HIV positive individuals under antiretroviral treatment in Shandong Province, China.
 PMID: 28750025       2017       PloS one
Result: A71T, A71AT, A71AV, L10I are PI minor resistance mutations.
Result: In the mutations identified at time of diagnosis, A71T, A71AT, A71AV, V179D, V106I, V106EIKV are polymorphic mutations.


  The infection staging and profile of genotypic distribution and drug resistance mutation among the human immunodeficiency virus-1 infected blood donors from five Chinese blood centers, 2012-2014.
 PMID: 28622345       2017       PloS one
Discussion: Perhaps a result that some polymorphic accessory mutations such as: A71V/T and L10I/V on PIs; V106I and V90I on NNRTIs, commonly observed in previous studies, were no longer classified as PI minor DRMs and NNRTI resistance mutations in the updated Stanford HIVdb Program Genotypic Resistance Interpretation Algorithm (HIVdb version 8.3).


  Identifications of drug resistance mutations among antiretroviral treatment naive HIV-1 patients in Peninsular Malaysia.
 PMID: 28107870       2017       Asian Pacific journal of tropical medicine
Abstract: RESULTS: DRMs were identified in 35% of patients, among which 46.7% of them showed minor resistance to protease inhibitor with A71V and L10l were the commonest DRMs detected.


  Prevalence of HIV-1 Subtypes and Antiretroviral Drug Resistance Mutations in Nepal.
 PMID: 27697032       2016       Current HIV research
Abstract: The minor protease inhibitors (PI) associated mutations (A71T/V and T74S) were observed in 5/35 (14.3%) subjects.


  Unique Flap Conformation in an HIV-1 Protease with High-Level Darunavir Resistance.
 PMID: 26870021       2016       Frontiers in microbiology
Table: A71V


  Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
 PMID: 27039930       2016       Biochemistry
Result: Unlike mutations V82S, proximal to the active site pocket, and G48V and I54V in the flap regions, non-active site mutations L90M and A71V may indirectly influence inhibitor or substrate binding.


  Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.
 PMID: 27992544       2016       PloS one
Abstract: Distal mutations A71V, L90M and I93L propagate alterations to the catalytic site of PRS17.
Result: A71V and L90M together are considered as resistance mutations for all clinical drugs except DRV and tipranavir.
Result: A71V in PRS17/DRV loses van der Waals contact with Leu89 but retains interaction with Gln92 in comparison to PR/DRV.



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