literature

IV mutation literature information.

Low replicative fitness of neuraminidase inhibitor-resistant H7N9 avian influenza a virus with R292K substitution in neuraminidase in cynomolgus macaques compared with I222T substitution.

PMID: 23951116 2013 PloS one

Introduction: The most common resistance mutations are H274Y (N2 numbering, this numbering is used throughout the paper) in the N1, and R292K or E119V in the N2 group.

Cell culture-selected substitutions in influenza A(H3N2) neuraminidase affect drug susceptibility assessment.

PMID: 24080660 2013 Antimicrobial agents and chemotherapy

Abstract: Sequence analysis of its NA gene revealed a known oseltamivir-resistance marker, the glutamic acid-to-valine substitution at position 119 (E119V), and an additional change, threonine to isoleucine at position 148 (T148I).

Abstract: Unlike E119V, T148I was not detected in the clinical sample but acquired during viral propagation in MDCK cells.

Generation and Characterization of Recombinant Influenza A(H1N1) Viruses Resistant to Neuraminidase Inhibitors.

PMID: 24524021 2013 Osong public health and research perspectives

Abstract: RESULTS: NA-inhibition assays showed that all the single and double mutants containing the Y275 except the single Y275-E119V mutant conferred important levels of resistance to oseltamivir, whereas all the single, double, and triple mutants containing the E119V mutation were associated with the resistance to zanamivir.

Method: To investigate mutations at NA key residues (N1 numbering: I117V, I117M, E119V, I223V, Y275H, R293K, N295S, and S334N), site-directed mutagenesis was conducted on the NA gene cloned plasmid using the Quic

The 2008-2009 H1N1 influenza virus exhibits reduced susceptibility to antibody inhibition: Implications for the prevalence of oseltamivir resistant variant viruses.

PMID: 22138712 2012 Antiviral research

Introduction: It was also shown that resistant mutants obtained through selection in culture or isolated from patients treated with neuraminidase inhibitors are subtype specific, with E119V and R292K NA mutations occurring mainly in H3N2 subtype viruses exposed to either oseltamivir or zanamivir, and the H275Y mutation in the NA protein found almost exclusively among H1N1 subtype viruses in response to oseltamivir treatment.

Rapid identification of neuraminidase inhibitor resistance mutations in seasonal influenza virus A(H1N1), A(H1N1)2009, and A(H3N2) subtypes by melting point analysis.

PMID: 22089329 2012 European journal of clinical microbiology & infectious diseases

Abstract: We evaluated the use of a procedure involving real-time polymerase chain reaction (PCR) followed by melting point analysis (MPA) of hybrids formed between the PCR product and a specific oligonucleotide probe for the identification of point mutations in the influenza A virus neuraminidase gene (NA) that are associated with oseltamivir resistance [resulting in the amino acid change H275Y for seasonal and pandemic influenza A(H1N1) viruses and E119V for A(H3N2) viruses].

Novel genotyping and quantitative analysis of neuraminidase inhibitor resistance-associated mutations in influenza a viruses by single-nucleotide polymorphism analysis.

PMID: 21730113 2011 Antimicrobial agents and chemotherapy

Abstract: The multi- or monoplex SNP analysis based on single nucleotide extension assays was developed to detect NA mutations H275Y and I223R/V in pandemic H1N1 viruses, H275Y in seasonal H1N1 viruses, E119V and R292K in seasonal H3N2 viruses, and H275Y and N295S in H5N1 viruses.

Combinatorial effect of two framework mutations (E119V and I222L) in the neuraminidase active site of H3N2 influenza virus on resistance to oseltamivir.

PMID: 21422222 2011 Antimicrobial agents and chemotherapy

Abstract: In MDCK-SIAT1 cells, the E119V+I222L mutant virus did not present a replicative advantage over the wild-type virus, even in the presence of oseltamivir.

Abstract: The E119V+I222L mutant was stable after five passages in MDCK cells.

Abstract: The total NA activity of the E119V+I222L mutant was low (5% compared to that of the wild-type virus).

The I222V neuraminidase mutation has a compensatory role in replication of an oseltamivir-resistant influenza virus A/H3N2 E119V mutant.

PMID: 21106781 2011 Journal of clinical microbiology

Abstract: Based on plaque size, yield assays, and NA activity, the impaired viral fitness of the E119V mutant was partially restored by the I222V NA mutation.

Abstract: Oseltamivir-resistant A/H3N2 influenza isolates with or without the E119V and I222V neuraminidase (NA) mutations were recovered from an immunocompromised patient.

Oseltamivir-resistant influenza A and B viruses pre- and postantiviral therapy in children and young adults with cancer.

PMID: 21048522 2011 The Pediatric infectious disease journal

Abstract: Three resistant influenza A (H3N2) viruses shared a common E119V NA mutation.

Introduction: E119V and N294S mutations occur in the framework region of the NA.

Introduction: In influenza viruses of the N2 subtype, a glutamic acid to valine substitution in residue 119 (E119V, N2 numbering here and through the text) confers resistance to oseltamivir but not to zanamivir; an arginine to lysine substitution at position 292 (R292K) confers resistance to both NAIs.

Clinical importance and impact on the households of oseltamivir-resistant seasonal A/H1N1 influenza virus in healthy children in Italy.

PMID: 20738882 2010 Virology journal

Abstract: The influenza A virus-positive samples underwent neuraminidase gene analysis using pyrosequencing to identify mutations H275Y and N294 S in A/H1N1, and E119V, R292K, and N294 S in A/H3N2.

Result: The A influenza virus-positive samples underwent neuraminidase gene analysis using pyrosequencing to identify mutations H275Y and N294 S in A/H1N1, and E119V, R292K, and N294 S in A/H3N2.

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