literature

HIV mutation literature information.

Gag P2/NC and pol genetic diversity, polymorphism, and drug resistance mutations in HIV-1 CRF02_AG- and non-CRF02_AG-infected patients in Yaounde, Cameroon.

PMID: 29074854 2017 Scientific reports

Method: Four subjects on ART also had viruses harboring the NNRTIs secondary mutations V179D, A98G, E138A, V179E, and F227L, including subject NA2CMR151 who had both A98G and the major NNRTI resistance mutation Y181C.

Virological response, HIV-1 drug resistance mutations and genetic diversity among patients on first-line antiretroviral therapy in N'Djamena, Chad: findings from a cross-sectional study.

PMID: 29126456 2017 BMC research notes

Abstract: Overall, 32% (37/116) patients presented >= one major drug resistant mutation(s), with 29% (34/116) to nucleos(t)ide reverse transcriptase inhibitors (67% [29/43] M184V/I, 30% [13/43] T215Y/F, 19% [8/43] V75A/F/I/L/M, 9% [4/43] K70P/R/W, 9% [4/43] K219E/N/Q and 5% [2/43] A62V); 86% (37/43) to non-nulceos(t)ide reverse transcriptase inhibitors (30% [13/43] K103N/S/E, 26% [11/43] Y181C/V/F/L, 2% [1/43] L100I, 2% [1/43] F227L, 2% [1/43] P225H); and 2% (1/43

Role of Rilpivirine and Etravirine in Efavirenz and Nevirapine-Based Regimens Failure in a Resource-Limited Country: A Cross- Sectional Study.

PMID: 27120449 2016 PloS one

Method: RT-RAMs were identified and analyzed by using the Stanford Drug Resistance Database for V90I, A98G, L100I/V, K101E/P/Q/H/N, K103N/S/T/Q/E/H/R, V106A/M/I, V108I, E138A/K/Q/G/R, V179D/E/T/F/L, Y181C/I/V/S/F/G, M184I, Y188C/H/L/F, G190A/S/E/Q/C/V/T, H221Y,

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.

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.

Rilpivirine and Doravirine Have Complementary Efficacies Against NNRTI-Resistant HIV-1 Mutants.

PMID: 27124362 2016 Journal of acquired immune deficiency syndromes (1999)

Result: In addition, the triple mutant V106A/G190A/F227L was relatively insensitive to DOR (>100 nM).

Result: Some of the viruses selected by DOR in culture contained additional mutations: V106A/F227L, V106A/L234I, and V106A/F227L/L234I.

Result: The double and triple mutants V106A/F227L, V106/L234I, and V106A/F227L/L234I all showed a substantial loss of susceptibility to DOR (>100 nM).

Rapid and Simultaneous Detection of Major Drug Resistance Mutations in Reverse Transcriptase Gene for HIV-1 CRF01_AE, CRF07_BC and Subtype B in China Using Sequenom MassARRAY(R) System.

PMID: 27092551 2016 PloS one

Table: F227L

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

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

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: F227L

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