literature

Molecular mechanism of HIV-1 resistance to 3'-azido-2',3'-dideoxyguanosine.

PMID: 24211331 2014 Antiviral research

Abstract: In this study, we have defined the molecular mechanisms of 3'-azido-ddG resistance by performing in-depth biochemical analyses of HIV-1 RT containing mutations L74V, F77L, V106I, L214F, R277K, and K476N (SGS3).

Abstract: Pre-steady-state kinetic experiments revealed that the L74V mutation allows RT to effectively discriminate between the natural nucleotide (dGTP) and 3'-azido-ddG-triphosphate (3'-azido-ddGTP).

Abstract: The L74V mutation was found to severely impair RT's ability to excise the chain-terminating 3'-azido-ddG-monophosphate (3'-azido-ddGMP) moiety.

Simultaneous detection of major drug resistance mutations in the protease and reverse transcriptase genes for HIV-1 subtype C by use of a multiplex allele-specific assay.

PMID: 23985909 2013 Journal of clinical microbiology

Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V,

PMID: 23068886 2013 Virology

Result: Since mutations in POL, especially L74V and M184V, can counteract AZT resistance levels, additional vectors were created in which the patient CNs were subcloned into pHL[C-TAMs].

Prevalence of primary resistance mutations to integrase inhibitors in treatment-naive and -experienced patients infected with B and non-B HIV-1 variants.

PMID: 23372110 2013 HIV clinical trials

Abstract: According to the geno2pheno algorithm, some of the secondary mutations detected (L74V, E138K, G163RS, and V151I) have been associated with a reduced estimated susceptibility to RAL and only the E138K mutation has been associated with a decreased estimated susceptibility to EGV.

Human APOBEC3G-mediated hypermutation is associated with antiretroviral therapy failure in HIV-1 subtype C-infected individuals.

PMID: 23443042 2013 Journal of the International AIDS Society

Table: L74V

Altered error specificity of RNase H-deficient HIV-1 reverse transcriptases during DNA-dependent DNA synthesis.

PMID: 23444139 2013 Nucleic acids research

Discussion: K65R, L74V, Q151N and M184I) have a relatively minor impact on error distribution, with frameshifts occurring mostly at nucleotide runs.

Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.

PMID: 23469241 2013 PloS one

Table: L74V/I

Restriction fragment mass polymorphism (RFMP) analysis based on MALDI-TOF mass spectrometry for detecting antiretroviral resistance in HIV-1 infected patients.

PMID: 23480551 2013 Clinical microbiology and infection

Abstract: The concordance rates between the RFMP and direct sequencing assays for the examined codons were 97% (K65R), 97% (T69Ins/D), 97% (L74VI), 97% (K103N), 96% (V106AM), 97% (Q151M), 97% (Y181C), 97% (M184VI) and 94% (T215YF) in the reverse transcriptase coding region, and 100% (D30N), 100% (M46I), 100% (G48V), 100% (I50V), 100% (I54LS), 99% (V82A), 99% (I84V) and 100% (L90M) in th

L74V increases the reverse transcriptase content of HIV-1 virions with non-nucleoside reverse transcriptase drug-resistant mutations L100I+K103N and K101E+G190S, which results in increased fitness.

PMID: 23535575 2013 The Journal of general virology

Abstract: However, L100I and K101E reduced the amount of RT in the virions and subsequent addition of L74V restored RT levels back to those of G190S or K103N alone.

Abstract: We conclude that fitness changes caused by L100I, K101E and L74V derive from their effects on RT content.

Abstract: We found that L100I, K101E and L74V did not change the polymerization or RNase H activities of K103N or G190S

PMID: 23717585 2013 PloS one

Table: L74V