IV mutation literature information.


  Simultaneous detection of oseltamivir- and amantadine-resistant influenza by oligonucleotide microarray visualization.
 PMID: 23451169       2013       PloS one
Abstract: Consequently, a cost-effective oligonucleotide microarray visualization method, which was based on quantum dot-catalyzed silver deposition, was developed and evaluated for the simultaneous detection of neuraminidase H275Y and E119V; matrix protein 2 V27A and S31N mutations of influenza A (H3N2), seasonal influenza A (H1N1), and 2009 influenza A (H1N1).
Introduction: Most N1 subtypes that are resistant to oseltamivir have been associated with the NA H275Y mutation, while N2 subtypes have been associated with the NA E119V mutation.
Introduction: The objective of this study was to design a cost-effective oligo


  Parallel screening of wild-type and drug-resistant targets for anti-resistance neuraminidase inhibitors.
 PMID: 23437217       2013       PloS one
Discussion: Many mutations of NAs have been reported including E119V, D151E, H275Y, R293K, and N295S.


  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].


  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.


  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.


  Surveillance of antiviral resistance markers in Argentina: detection of E119V neuraminidase mutation in a post-treatment immunocompromised patient.
 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).


  Surveillance of antiviral resistance markers in Argentina: detection of E119V neuraminidase mutation in a post-treatment immunocompromised patient.
 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.


  Oseltamivir-resistant pandemic H1N1/2009 influenza virus possesses lower transmissibility and fitness in ferrets.
 PMID: 20686654       2010       PLoS pathogens
Introduction: These studies differed in the influenza A subtypes studied (H1N1, H3N2, or H5N1), the NA mutations involved (H275
Discussion: The only study to date that has evaluated both routes of transmission of oseltamivir-resistant virus showed that recombinant resistant H3N2 viruses with either the E119V or the E119V+I222V NA mutation were transmitted efficiently by direct contact but not by respiratory droplets among guinea pigs.
Discussion: Under similar conditions, the transmission of an E119V mutant of H3N2 virus and an H275Y mutant of A/New Caledonia/20/99-like (H1N1) virus by direct contact required a higher dose of inoculum than transmission of the wild-type viruses, and it occurred more slowly.



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