literature

HIV mutation literature information.

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.

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.

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

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.

HIV type 1 drug resistance patterns among patients failing first and second line antiretroviral therapy in Nairobi, Kenya.

PMID: 25487529 2014 BMC research notes

Abstract: In addition, among patients failing second-line (20), six patients (30%) had NNRTI resistance; two patients on K103N and G190A mutations while V106A, Y184V, A98G, Y181C mutations per patient were also detected.

Result: Single occurring mutations of V106A occurred as expected in a patient who had NVP regimen.

Result: These mutations were M184V (n = 1), T215Y (n = 2), V106A (n = 1), A98G (n = 1), Y18C1C (n = 1), G190A (n = 1) and V108IV (n = 1).

The development of drug resistance mutations K103N Y181C and G190A in long term Nevirapine-containing antiviral therapy.

PMID: 25926857 2014 AIDS research and therapy

Discussion: The rank of fitness among mutant viruses was as follows: wild type (WT) >= Y181C >= K103N >= G190A >= V106A >= P236L >= G190S.

HIV-1 virologic failure and acquired drug resistance among first-line antiretroviral experienced adults at a rural HIV clinic in coastal Kenya: a cross-sectional study.

PMID: 24456757 2014 AIDS research and therapy

Table: V106A

Non-nucleoside reverse transcriptase inhibitor (NNRTI) cross-resistance: implications for preclinical evaluation of novel NNRTIs and clinical genotypic resistance testing.

PMID: 23934770 2014 The Journal of antimicrobial chemotherapy

Abstract: RESULTS: Sixteen mutations at 10 positions were significantly associated with the greatest contribution to reduced phenotypic susceptibility (>=10-fold) to one or more NNRTIs, including: 14 mutations at six positions for nevirapine (K101P, K103N/S, V106A/M, Y181C/I/V, Y188C/L and G190A/E/Q/S); 10 mutations at six positions for efavirenz (L100I, K101P, K103N, V106M, Y188C/L and G190A/E/Q/S); 5 mutations at four positions for etravirine (

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