literature

IV mutation literature information.

Tracking oseltamivir-resistance in New Zealand influenza viruses during a medicine reclassification in 2007, a resistant-virus importation in 2008 and the 2009 pandemic.

PMID: 23908945 2012 Western Pacific surveillance and response journal

Abstract: Sequencing of the neuraminidase gene showed that the resistant viruses contained an H275Y mutation, and S247N was also identified in the neuraminidase gene of one seasonal influenza A(H1N1) virus that exhibited enhanced resistance.

Genetic and phylogenetic analyses of influenza A H1N1pdm virus in Buenos Aires, Argentina.

PMID: 21047959 2011 Journal of virology

Abstract: The N-4 fragment as well as the hierarchical clustering of samples showed that a consensus sequence prevailed in time but also that different variants, including five H275Y oseltamivir-resistant strains, arose from May to August 2009.

Pandemic H1N1 2009 influenza virus with the H275Y oseltamivir resistance neuraminidase mutation shows a small compromise in enzyme activity and viral fitness.

PMID: 21172786 2011 The Journal of antimicrobial chemotherapy

Abstract: BACKGROUND: Resistance to the neuraminidase inhibitor oseltamivir can be conferred by a well-characterized mutation in the neuraminidase gene, H275Y.

Abstract: CONCLUSIONS: The neuraminidase protein of pandemic influenza isolates tolerates the H275Y mutation and this mutation confers resistance to oseltamivir.

Abstract: METHODS: Using reverse genetics we engineered the H275Y mutation into the neuraminidase of a 2009 pandemic H1N1 virus and assessed the ability of this enzyme to desialylate mono- and multivalent substrates.

Nationwide molecular surveillance of pandemic H1N1 influenza A virus genomes: Canada, 2009.

PMID: 21249207 2011 PloS one

Result: These variants were V83M (1); S95G (4); V106I (49); E119K (1); I163V (1); I188V (1); N189S (1); V264I (1); H275Y (5); S286G (16); E287K (1); N295S (1); T332A (2); S388L (1); V394I (17), and E462G (1) (summarized in Table S2).

Discussion: The neuraminidase H275Y (H274Y in N2 numbering) mutation known to confer resi

Development of a real-time RT-PCR assay for detection of resistance to oseltamivir in influenza A pandemic (H1N1) 2009 virus using single nucleotide polymorphism probes.

PMID: 21349290 2011 Journal of virological methods

Abstract: The limit of detection was 47.6 copies/reaction for wild-type H275 RNA and 52.9 copies/reaction for the mutant H275Y RNA.

Discussion: As there are still some questions as to whether or not this H275Y polymorphism impairs viral fitness and transmission, we must be prepared for the possibility that oseltamivir-resistant isolates of the pandemic (H1N1) 2009 virus could expand in a manner similar to that seen in the previous seasonal H1N1 viruses.

Discussion: Given the concerns about how H275Y SNP assays perform in the context of mixed viral populations and mutations in the probe-binding region, the authors feel that the results of a SNP assay should be interpreted with caution and ambiguous results should be confirmed by sequencing.

Discussion: In conclusion, this manuscript describes the development and validation of a SNP assay for the detection of

PMID: 21427949 2011 Voprosy virusologii

Abstract: All the test strains contain the S31N substitution in the M2 protein, which determines viral resistance to adamantine, and have no H275Y substitution in neuraminidase, which determines oseltamivir resistance.

Assessing the in vitro fitness of an oseltamivir-resistant seasonal A/H1N1 influenza strain using a mathematical model.

PMID: 21455300 2011 PloS one

Abstract: Although previous studies had demonstrated that this mutation impaired the replication capacity of the influenza virus in vitro and in vivo, the A/Brisbane/59/2007 H275Y oseltamivir-resistant mutant completely out-competed the wild-type (WT) strain and was, in the 2008-2009 influenza season, the primary A/H1N1 circulating strain.

Abstract: In 2007, the A/Brisbane/59/2007 (H1N1) seasonal influenza virus strain acquired the oseltamivir-resistance mutation H275Y in its neuraminidase (NA) gene.

Abstract: In the ST6GalI-MDCK cell line, the latent infection period (i.e., the time for a newly infected cell to start releasing virions) was found to be 1-3 h for the WT strain and more than 7 h for the H275Y mutant.

Ultrasensitive detection of drug-resistant pandemic 2009 (H1N1) influenza A virus by rare-variant-sensitive high-resolution melting-curve analysis.

PMID: 21543559 2011 Journal of clinical microbiology

Abstract: Although a majority of 2009 (H1N1) influenza A virus remains oseltamivir susceptible, the threat of resistance due to the His275Tyr mutation is highlighted by the limitations of alternative therapies and the potential for rapid, global fixation of this mutation in the circulating influenza A virus population.

Abstract: In order to better understand the emergence of resistance, we developed a rare-variant-sensitive high-resolution melting-curve analysis method (RVS-HRM) that is able to detect the His275Tyr oseltamivir resistance mutation to 0.5% in a background of susceptible virus.

Mutation analysis of 2009 pandemic influenza A(H1N1) viruses collected in Japan during the peak phase of the pandemic.

PMID: 21572517 2011 PloS one

Abstract: Oseltamivir resistance-related mutations, i.e., NA-H275Y and NA-N295S, were also detected in sporadic cases in Osaka and Tokyo.

Result: In our clinical study carried out in Tokyo, the NA-H275Y mutation was found in a patient (6 years old) who had influenza-induced brain edema and severe pneumonia with little response to oseltamivir (4 mg/kg/day).

Result: Oseltamivir-resistance associated mutations: H275Y and N295S in NA.

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 SNP analysis revealed the lower growth fitness of an H

Abstract: The monoplex assays for the H275Y NA mutation allowed precise and accurate quantification of the proportions of wild-type and mutant genotypes in virus mixtures (5% to 10% discrimination), with results comparable to those of pyrosequencing.

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.

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