HIV mutation literature information.


  Polymorphisms and Mutational Covariation Associated with Death in a Prospective Cohort of HIV/AIDS Patients Receiving Long-Term ART in China.
 PMID: 28099515       2017       PloS one
Result: For example, M41L and D67N had 16 (D218E, E44A, G190S, G196E, H221Y, I142V, K101E, L210W, L228R, L74V, M184V, R211K, T215F, V108I, V118I, and V179I) and nine (E44A, H208Y, H221Y, K70R, L210W


  HIV-1 drug-resistant mutations and related risk factors among HIV-1-positive individuals experiencing treatment failure in Hebei Province, China.
 PMID: 28114955       2017       AIDS research and therapy
Table: V108I


  HIV Drug Resistance Mutations in Non-B Subtypes After Prolonged Virological Failure on NNRTI-Based First-Line Regimens in Sub-Saharan Africa.
 PMID: 28129253       2017       Journal of acquired immune deficiency syndromes (1999)
Discussion: To our knowledge, the differences we found in the other NNRTI DRMs, K101E (rilpivirine and etravirine resistance), Y181C (resistance to all NNRTIs), V108I (efavirenz and nevirapine resistance), and P225H (efavirenz resistance) have not been reported previously.


  High level of HIV-1 drug resistance mutations in patients with unsuppressed viral loads in rural northern South Africa.
 PMID: 28750647       2017       AIDS research and therapy
Table: V108I


  Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
 PMID: 28891788       2017       HIV clinical trials
Method: Primary NNRTI-R substitutions assessed were V90I, A98G, L100I, K101E/H/P, K103N/S, V106A/I/M, V108I, E138A/G/K/Q/R, V179D/F/L/T, Y181C/I/V, Y188C/H/L, G190A/E/Q/S, H221Y, P225H, F227C, and M230I/L in RT.


  HIV drug resistance in HIV positive individuals under antiretroviral treatment in Shandong Province, China.
 PMID: 28750025       2017       PloS one
Result: V108A is a highly unusual mutation at the position of 108, where usually is V108I, a non-polymorphic accessory mutation.
Table: V108I


  Prevalence of Drug Resistance Associated Mutations Among the Anti Retroviral Therapy Exposed HIV-1 Infected Individuals in Manipur, Northeast India.
 PMID: 27033350       2016       Current HIV research
Abstract: Predominant DRAMs at RT genes were M184V, T215Y, M41L and V108I and H221Y while at PR genes were M46I and I47V.


  Prevalence of Primary HIV Drug Resistance in Thailand Detected by Short Reverse Transcriptase Genotypic Resistance Assay.
 PMID: 26828876       2016       PloS one
Abstract: Fourteen major mutations of codon 99-191 on the RT gene were selected (K103N, V106A/M, V108I, Q151M, Y181C/I, M184V/I, Y188C/L/H, and G190S/A) at a cost of testing of 35 USD.
Abstract: The prevalence of each HIVDR mutation were K103N 6.0%, V106I 1.1%, V108I 0.4%, Y181C 2.3%, Y181I 0.7%, Y181V 0.4%, M184V 3.0%, M184I 1.5%, and  PMID: 26651266       2016       AIDS research and human retroviruses
Method: In addition, we defined a list of minor RPV-RAMs that have been observed in in vitro or in vivo selection studies and are included in one or more of clinically widely used genotypic resistance interpretation algorithms ANRS (V24), Rega (V9.1.0), and HIVdb (V7.0.1), encompassing V90I, A98G, L100I/V, K101H/Q/T, K103R/S, V106A/I, V108I, E138S, V179D/E/F/I/T, Y181F/G/S, Y188F, V189I, G190A/C/E/Q/S/T/V, and M230V


  Discovery, characterization, and lead optimization of 7-azaindole non-nucleoside HIV-1 reverse transcriptase inhibitors.
 PMID: 27390064       2016       Bioorganic & medicinal chemistry letters
Introduction: Both drugs selected for mutations on RT, as the V108I mutant emerged after 69 weeks of treatment with 8 and E138K arose after 39 weeks of treatment with 9 (Supp.
Introduction: However, none of the compounds inhibited the V108I mutant selected by 8, indicating that there may be conserved binding features among all three molecules that are disrupted by this mutation.
Introduction: It did demonstrate some potency against the Y181C RT mutant in the cell-free assay (IC50 = 6.69 muM, data not shown), but was inactive against the K103N, V108I, and E138 K forms of the enzyme.



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