literature

HIV mutation literature information.

Prevalence in the USA of rilpivirine resistance-associated mutations in clinical samples and effects on phenotypic susceptibility to rilpivirine and etravirine.

PMID: 24704709 2014 Antiviral therapy

Abstract: METHODS: In total, 15,991 samples submitted to Monogram Biosciences (South San Francisco, CA, USA) for routine resistance testing between January 2010 and June 2011 were assessed for the presence of known rilpivirine RAMs K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L; non-nucleoside reverse transcriptase inhibitor (NNRTI) RAMs K103N, L100I and L100I+K103N; and the

Differential impact of APOBEC3-driven mutagenesis on HIV evolution in diverse anatomical compartments.

PMID: 24401644 2014 AIDS (London, England)

Abstract: G73S in protease; M184I, M230I in reverse transcriptase) and two other patients' rectal tissues (M184I, M230I in reverse transcriptase) while such mutations were absent from paired peripheral blood mononuclear cells.

Prevalence of pre-existing resistance-associated mutations to rilpivirine, emtricitabine and tenofovir in antiretroviral-naive patients infected with B and non-B subtype HIV-1 viruses.

PMID: 23361642 2013 The Journal of antimicrobial chemotherapy

Abstract: We studied the primary rilpivirine RAMs (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, H221Y, F227C and M230I/L) and other potential rilpivirine-associated mutations (V90I, L100I, K101T, E138S, V179D/I, Y188L, V189I, G190A/E/S and M230V).

Rilpivirine: a new non-nucleoside reverse transcriptase inhibitor.

PMID: 23099850 2013 The Journal of antimicrobial chemotherapy

Abstract: Seventeen NNRTI mutations have been associated with decreased susceptibility to rilpivirine: K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, H221Y, F227C, M230I/L, Y188L and the combination L100I + K103N.

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

Abstract: In therapy-naive individuals, hypermutated proviral DNA with M184I and M230I mutations due to the editing of hA3G, had stop codons in the open reading frames and the same mutations were absent in the plasma virus.

Abstract: It is unlikely that viral variants, which exhibit hypermutated sequences and M184I and/or M230I, will mature and expand in vivo.

Result: The three hypermutated proviral sequences from the therapy naive patients who had M184I and M230I drug resistance mutations and mutation in drug resistance position (M41I) also had stop codons in the RT ORF particularly at the tryptophan residue, which is the target site for hA3G.

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

PMID: 23444139 2013 Nucleic acids research

Introduction: In addition, other mutants such as M230I and M230L were prone to introduce tandem repeat deletions, particularly in the presence of biased dNTP concentrations.

[Resistance profile of rilpivirine].

PMID: 24252532 2013 Enfermedades infecciosas y microbiologia clinica

Abstract: In vitro studies and phase III clinical trials have allowed the identification of 16 mutations associated with resistance to RPV K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L.

Lys66 residue as a determinant of high mismatch extension and misinsertion rates of HIV-1 reverse transcriptase.

PMID: 22925131 2012 The FEBS journal

Discussion: Several substitutions at residues that do not directly line the active site, but yet impinge upon it via interaction with template or primer, such as Met230Ile (in the primer grip) and Glu89Gly (at -2 position on the template) have also been shown to bring about increases in fidelity.

The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains.

PMID: 21569325 2011 Retrovirology

Introduction: The replicative capacity of a Q151L-containing virus was shown to improve in the presence of S68G and M230I mutations suggesting that compensatory mutations could favour the emergence of the Q151M MDR complex.

K65R and K65A substitutions in HIV-1 reverse transcriptase enhance polymerase fidelity by decreasing both dNTP misinsertion and mispaired primer extension efficiencies.

PMID: 20538005 2010 Journal of molecular biology

Discussion: The Y115W substitution also reduces dNTP binding affinity and decreases primer mismatch extension, although this effect can be somewhat mitigated by the presence of a primer-grip substitution, M230I.

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