Abstract: Predominant DRAMs at RT genes were M184V, T215Y, M41L and V108I and H221Y while at PR genes were M46I and I47V.
Treatment failure and drug resistance in HIV-positive patients on tenofovir-based first-line antiretroviral therapy in western Kenya.
PMID: 27231099
2016
Journal of the International AIDS Society
Table: V108I
HIV-1 Drug Resistance by Ultra-Deep Sequencing Following Short Course Zidovudine, Single-Dose Nevirapine, and Single-Dose Tenofovir with Emtricitabine for Prevention of Mother-to-Child Transmission.
PMID: 27327263
2016
Journal of acquired immune deficiency syndromes (1999)
Result: Mutations conferring low to intermediate NNRTI resistance included K101E in 7 of 26 (27%), A98G 5 of 26 (19%), L100V 4 of 26 (15%), V108I in 1 of 26 (3%) and F227L in 1 of 26 (3%) of patients.
Treatment Outcomes and Resistance Patterns of Children and Adolescents on Second-Line Antiretroviral Therapy in Asia.
PMID: 27355415
2016
Journal of acquired immune deficiency syndromes (1999)
Result: Of the 156 (56%) children who had available resistance testing at the time of first-line failure, mutations included M184V (82%), >=1 thymidine analog mutation (TAM; 64%), >=4 TAMs (18%), T215Y/F (43%), K65R (10%), >=1 NNRTI mutation (92%), Y181I/C (44%), G190A (33%), K103N/S (27%), and V108I (15%); 30 (19%) children had DUET weighted scores >=4 (Table 2).
Accumulation of HIV-1 drug resistance after continued virological failure on first-line ART in adults and children in sub-Saharan Africa.
PMID: 27342546
2016
The Journal of antimicrobial chemotherapy
Abstract: RESULTS: At first virological failure, DRM(s) were detected in 87% of participants: K103N (38.7%), G190A (21.8%), Y181C (20.2%), V106M (8.4%), K101E (8.4%), any E138 (7.6%) and V108I (7.6%) associated with NNRTIs, and M184V (69.7%), any thymidine analogue mutation (9.2%), K65R (5.9%) and K70R (5.0%) associated with NRTIs.
HIV-1 Epidemiology, Genetic Diversity, and Primary Drug Resistance in the Tyumen Oblast, Russia.
Result: The mutations with a low effect on the resistance to NNRTIs (E138A, V108I, and V90I) also had a low prevalence.
Discussion: Mutations K103N, M184I, T215Y, G190S, Y181C, K65R, and V108I with prevalences of 0.3 to 7% depending on the region are most frequently detected in the naive HIV-infected individuals.
Viral and Host Characteristics of Recent and Established HIV-1 Infections in Kisumu based on a Multiassay Approach.
Abstract: Overall, HIV-1 subtype A (63%), D (15%), C (3%), G (1%) and recombinants (18%), two monophyletic dyads and intrinsic viral mutations (V81I, V81I/V, V108I/V and K101Q) were observed.
Result: Observed viral mutations included V81I and V81I/V in the protease gene, and V108I/V and K101Q in the reverse transcriptase gene, all of which were intrinsic mutations not associated with ARV exposure.
HIV Drug Resistance in Antiretroviral Treatment-Naive Individuals in the Largest Public Hospital in Nicaragua, 2011-2015.
Result: This increase was mainly NNRTI-associated due to the presence of the polymorphic mutation E138A (86% of cases) and to a lesser extent V108I (14% of cases), which are not considered in the SDRMs list.
Prevalence of HIV Antiretroviral Drug Resistance and Its Impacts on HIV-1 Virological Failures in Jiangsu, China: A Cross-Sectional Study.
Result: K103N, Y181C, G190A, and V108I were the most prevalent mutations associated with NNRTIs resistance and the frequencies were 33.70%, 29.35%, 27.17%, and 27.17%, respectively (Figure 2(b)).
Discovery, characterization, and lead optimization of 7-azaindole non-nucleoside HIV-1 reverse transcriptase inhibitors.
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.
Introduction: The three most active compounds against wild type