In vitro selection of HIV-1 CRF08_BC variants resistant to reverse transcriptase inhibitors.
PMID: 25482475
2015
AIDS research and human retroviruses
Abstract: Initial mutations, in combination with other previously reported substitutions (K20R, D67N, V90I, K101R/E, V106I/A, V108I, F116L, E138R, A139V, V189I, G190A, D218E, E203K, H221Y, F227L, N348I, and T369I) or novel mutations (V8I, S134N, C162Y, L228I
Viral Genetic Diversity and Polymorphisms in a Cohort of HIV-1-Infected Patients Eligible for Initiation of Antiretroviral Therapy in Abuja, Nigeria.
PMID: 25582324
2015
AIDS research and human retroviruses
Result: Five specimens had A98G, K101EK, V108IV, K103N, E138A, and G190A occurring alone or in combination with each other, which could cause intermediate and/or high-level resistance to delavirdine (DLV), efavirenz (EFV), etravirine (ETR), and nevirapine (NVP).
Result: We also detected NRTI selected mutations M41L, E44D, T69ANS, V75M, and V118I, and NNRTI mutations V90I, A98G, K101EQ, PMID: 25754408
2015
Journal of medical virology
Result: The most prevalent NNRTI mutations were Y181C/I/V (n = 24, 35%), (n = 3, 4%), and (n = 1 (1%), respectively, K103N/S (n = 21 (32%) and n = 1 [1%]), G190A/S/E (n = 20 (29%), n = 1 (1%), and (n = 2, 3%), respectively, V108I (n = 13, 19%), and V106A/M (n = 2, 3%) and (n = 10, 15%).
Geographic and temporal trends in the molecular epidemiology and genetic mechanisms of transmitted HIV-1 drug resistance: an individual-patient- and sequence-level meta-analysis.
Result: Nevirapine and efavirenz resistance were predicted in about 1% and 0.5% of virus samples without NNRTI SDRMs as a result of several minimally polymorphic (e.g., A98G, V108I, and V179D) and rare nonpolymorphic (e.g., E138K, G190Q, F227C, and K238T) NNRTI-resistance mutations.
Single Genome Analysis for the Detection of Linked Multiclass Drug Resistance Mutations in HIV-1-Infected Children After Failure of Protease Inhibitor-Based First-Line Therapy.
PMID: 25923117
2015
Journal of acquired immune deficiency syndromes (1999)
8Discussion: Our evidence also points to the triple-class drug-resistant variants detected in ""J"" to be a result of genetic ""hitchhiking"" by V108I."
Result: Emergence of V108I after ART initiation was not statistically supported (P = 0.189 for test of proportions of genomes carrying V108I between baseline and week 298).
Result: The NNRTI mutation V108I was first detected at week 96 of ART at a frequency of 3% and again detected at a frequency of 5% at week 298 (Table 3).
Result: The variant contained M184V, V108I in RT, and M46I in PR (Table 5).
Discussion: V108I is known to
Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.
Method: A NVP RAM was considered if at least one of the following genetic changes in reverse transcriptase was detected: A98G, K101E, K101H, K101P, K103N, V106A, V106M, V108I, Y181C, Y181V, Y188L and G190A.
Result: There were also multiple occurrences of V108I (n = 6), A98G (n = 6), K101E (n = 4), V106A (n = 4), K101P (n = 1).
Comparison of 454 Ultra-Deep Sequencing and Allele-Specific Real-Time PCR with Regard to the Detection of Emerging Drug-Resistant Minor HIV-1 Variants after Antiretroviral Prophylaxis for Vertical Transmission.
Result: Twenty-eight NVP-selected mutations (V90I, K101E, K103N/R, V106A/I/M, V108I, E138A/G/K/R, Y181C, Y188C, G190A or P225H) were detected in 19 samples at levels of 1.1% to 99.1%.
Table: V108I
HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.
HIV mutation literature information.
PMID: 
2015
AIDS research and human retroviruses
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