literature

HIV mutation literature information.

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: Of all mutations conferring resistance to NNRTIs, the most common were those conferring high-level NNRTI resistance such as K103N in 8 of 26 (30%), V106M in 8 of 26 (30%), Y188C in 6 of 26 (23%), G190A in 4 of 26 (15%), Y181C in 3 of 26 (11%), and V106A in 3 of 26 (11%) patients.

Cross-sectional study of virological failure and multinucleoside reverse transcriptase inhibitor resistance at 12 months of antiretroviral therapy in Western India.

PMID: 27631260 2016 Medicine

Discussion: The most common NRTI mutations reported were M184V and K65R whereas K103N/S and V106A/M were common NNRTI resistance mutations.

Design, Synthesis, and Evaluation of Thiophene[3,2-d]pyrimidine Derivatives as HIV-1 Non-nucleoside Reverse Transcriptase Inhibitors with Significantly Improved Drug Resistance Profiles.

PMID: 27541578 2016 Journal of medicinal chemistry

Abstract: Compound 27 was the most potent; compared with ETV, its antiviral efficacy was 3-fold greater against WT, 5-7-fold greater against Y181C, Y188L, E138K, and F227L+V106A, and nearly equipotent against L100I and K103N, though somewhat weaker against K103N+Y181C.

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: V106A

In vitro resistance selection with doravirine (MK-1439), a novel nonnucleoside reverse transcriptase inhibitor with distinct mutation development pathways.

PMID: 25385110 2015 Antimicrobial agents and chemotherapy

Abstract: In the resistance selection of subtype A and C viruses, similar mutation development pathways were detected, in which a V106A or V106M mutant was also the starting virus in the pathways.

Abstract: In the resistance selection of subtype B virus with DOR, a V106A mutant virus led to two mutation pathways, followed by the emergence separately of either F227L or L234I.

Abstract: When the replication capacity of the V106A mutant was compared with that of the wild-type (WT) virus, the mutant virus was 4-fold less fit than the WT virus.

High level of HIV-1 drug resistance among patients with HIV-1 and HIV-1/2 dual infections in Guinea-Bissau.

PMID: 25889017 2015 Virology journal

Table: V106A

Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.

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%).

Mutations in the reverse transcriptase and protease genes of human immunodeficiency virus-1 from antiretroviral naive and treated pediatric patients.

PMID: 25674767 2015 Viruses

Table: V106A

Discussion: Two ART naive patients, AIIMSU63 and AIIMSPD5 harbored L74I (conferring high level of resistance to didanosine; NNRTI inhibitor) and V106A (conferring high level of resistance to nevirapine; NNRTI inhibitors) mutations respectively.

Next generation sequencing improves detection of drug resistance mutations in infants after PMTCT failure.

PMID: 25542470 2015 Journal of clinical virology

Result: For the infant with K103N, detected by bulk sequencing, both Ion PGM and MiSeq additionally detected V106A/M and Y181C DRMs.

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

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