literature

Antiretroviral drug resistance in HIV-2: three amino acid changes are sufficient for classwide nucleoside analogue resistance.

PMID: 19358668 2009 The Journal of infectious diseases

Result: 3.1 +- 0.3 mumol/L, for Q151M and Q151M+3, respectively), indicating that A62V, F77L, and Y116F do not enhance AZT resistance in HIV-2.

Result: Although A62V, F77L, and Y116F increase the level of Q151M-mediated AZT resistance in HIV-1, the Q151M and Q151M+3 variants of HIV-2ROD exhibited comparable sensitivity to the drug (mean EC50 [+-SD], 5.2 +- 2.3 vs.

Result: Surprisingly, the dose-response profile of Q151M HIV-2ROD was comparable to that of the highly resistant Q151M/A62V/

PMID: 18487070 2008 The international journal of biochemistry & cell biology

Abstract: EFdA retains potency toward many HIV-1 resistant strains, including the multi-drug resistant clone HIV-1A62V/V75I/F77L/F116Y/Q151M.

Mutations at 65 and 70 within the context of a Q151M cluster in human immunodeficiency virus type 1 reverse transcriptase impact the susceptibility to the different nucleoside reverse transcriptase inhibitors in distinct ways.

PMID: 17567542 2007 Infection, genetics and evolution

Abstract: The original isolate carried the MNR mutations S68G, V75I, F77L, F116Y and Q151M, the lamivudine mutation M184V, the NNRTI mutation K103N and the yet unreported K70S.

HIV-1 subtype B protease and reverse transcriptase amino acid covariation.

PMID: 17500586 2007 PLoS computational biology

Method: NRTI-selected mutations included T39A, M41L, K43E/Q/N, E44D/A, A62V, K65R, D67N/G/E, T69D/N/S/insertion, K70R, L74V/I, V75I/M/T/A, F77L, V90I, K104N, Y115F, F116Y, V118I, Q151M, M184V/I, E203K,

PMID: 16048947 2005 Antimicrobial agents and chemotherapy

Abstract: In contrast, the susceptibility of the virus carrying the K65R mutation or the multidrug-resistant mutation with the Q151M complex (A62V, V75I, F77L, F116Y, and Q151M) was not altered.

Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.

PMID: 19825125 2005 Journal of the International AIDS Society

Table: F77L

Drug-resistance mutations in antiretroviral-naive patients with established HIV-1 infection in Mexico.

PMID: 16268822 2005 HIV medicine

Abstract: For nucleoside inhibitors, mutations T215Y/C and F77L (3%) and D67N/S, T69N and M184V (2%), were detected.

Effects of HIV Q151M-associated multi-drug resistance mutations on the activities of (-)-beta-D-1',3'-dioxolan guanine.

PMID: 15885814 2005 Antiviral research

Abstract: At the enzyme level, the addition of the A62V mutation to V75I/F77L/F116Y/Q151M moderately (3.4-fold) reversed the resistance to DXG-TP.

Abstract: In this study, we evaluated the antiviral activity of (-)-beta-D-1',3'-dioxolan guanine (DXG) towards mutant HIV-1 containing V75I/F77L/F116Y/Q151M (V75Icomplex) and A62V/V75I/F77L/F116Y/Q151M (A62Vcomplex) in MT-2 cells.

Abstract: The multi-drug resistance HIV-1 genotype A62V/V75I

Transmitted human immunodeficiency virus type 1 carrying the D67N or K219Q/E mutation evolves rapidly to zidovudine resistance in vitro and shows a high replicative fitness in the presence of zidovudine.

PMID: 15220429 2004 Journal of virology

Abstract: Of these viruses, 9 (25.7%) had only secondary TAMs (D67N, K219Q, M41L, or F77L), and all were found to be sensitive to zidovudine (AZT) and other drugs.

The molecular mechanism of multidrug resistance by the Q151M human immunodeficiency virus type 1 reverse transcriptase and its suppression using alpha-boranophosphate nucleotide analogues.

PMID: 12194983 2002 The Journal of biological chemistry

Abstract: The appearance of up to five substitutions (A62V, V75I, F77L, F116Y, and Q151M) in the viral reverse transcriptase promotes resistance to these drugs, and reduces efficiency of the antiretroviral chemotherapy.

Abstract: Using A62V/V75I/F77L/F116Y/Q151M RT, k(pol) increases up to 70- and 13-fold using alpha-boranophosphate-ddATP and alpha-boranophosphate AZTTP, respectively.

Abstract: Using pre-steady state kinetics, we show that Q151M and A62V/