Rapid quantification of single-nucleotide mutations in mixed influenza A viral populations using allele-specific mixture analysis.
PMID: 19761797
2010
Journal of virological methods
Abstract: The FluASMA assays target L26F, V27A, A30T, and S31N mutations in the A/Albany/1/98 (H3N2) M2 gene and H275Y mutation in the A/New Caledonia/20/99 (H1N1) NA gene and have a limit of quantification of 0.25-0.50% mutant.
Evaluation of a rapid molecular algorithm for detection of pandemic influenza A (H1N1) 2009 virus and screening for a key oseltamivir resistance (H275Y) substitution in neuraminidase.
Abstract: In addition, we investigated the performance of a novel discrimination RT-PCR for detection of the H275Y resistance mutation in the neuraminidase gene.
Abstract: Specificity and discriminative capacities of the H275Y discrimination assay were performed by testing wild type and recombinant H275Y pandemic influenza.
Method: At position 823 of pJET1.2-NA-H275Y, the cytosine was replaced by a thymine, resulting in the mutant sequence.
Method: For the evaluation of the primers and probes for the H275Y discrimination assay, two plasmids pJET1.2-NA-H275H and pJET1.2-NA-H275Y were constr
Host cell selection of influenza neuraminidase variants: implications for drug resistance monitoring in A(H1N1) viruses.
Abstract: Pyrosequencing analysis confirmed H274Y mutation (H275Y in N1 numbering) in the neuraminidase (NA) gene of oseltamivir-resistant viruses.
Detection of molecular markers of drug resistance in 2009 pandemic influenza A (H1N1) viruses by pyrosequencing.
PMID: 20028826
2010
Antimicrobial agents and chemotherapy
Abstract: We report on the detection of the first cases of the oseltamivir resistance-conferring mutation H275Y and the I223V change in viruses from the United States using the approach described in this study.
Genetic makeup of amantadine-resistant and oseltamivir-resistant human influenza A/H1N1 viruses.
PMID: 20129961
2010
Journal of clinical microbiology
Abstract: Phylogenetic analysis revealed that the oseltamivir-resistant strain evolved from a reassortant oseltamivir-susceptible strain (clade 2B) which circulated in the 2007-2008 season by acquiring the H275Y resistance-conferring mutation in the NA gene.
Abstract: Therefore, a reassortment event involving two distinct oseltamivir-susceptible lineages, followed by the H275Y substitution in the NA gene and other mutations elsewhere in the genome, contributed to the emergence of the oseltamivir-resistant lineage.
Oseltamivir-induced resistant pandemic A/H1N1 influenza virus in a child with cystic fibrosis and Pseudomonas aeruginosa infection.
Abstract: Infection due to pandemic virus with the H275Y mutation can be associated with a severe clinical course, supporting the systematic monitoring of antiviral susceptibility in pandemic influenza-positive high-risk patients whose influenza is not resolved by oseltamivir treatment.
Detection of the rapid emergence of the H275Y mutation associated with oseltamivir resistance in severe pandemic influenza virus A/H1N1 09 infections.
Abstract: From 25 patients who had been treated with oseltamivir and remained A/H1N1 09 RT-PCR positive, we identified three (12%) individuals with the H275Y mutation: one immuno-suppressed adult, one immuno-competent adult and one child.
Abstract: Most isolates of the new A/H1N1 09 virus are susceptible to neuraminidase inhibitors, but the H275Y mutation in the neuraminidase gene region associated with high-level oseltamivir resistance has been detected.
Abstract: RCA demonstrates the rapid emergence of the H275Y resistance mutation in individuals with severe A/H1N1 09 infection receiving neuraminidase inhibitors.
Abstract: Using rolling circle amplification (RCA) technology, 96 A/H1N1 09-specific RT
Antiviral drug susceptibilities of seasonal human influenza viruses in Lebanon, 2008-09 season.
Abstract: All the H3N2 viruses were resistant to amantadine but were sensitive to oseltamivir and zanamivir; while all the H1N1 viruses were resistant to oseltamivir (possessed H275Y mutation, N1 numbering, in their NA) but were sensitive to amantadine and zanamivir.
Epidemiological, demographic, and molecular characteristics of laboratory-confirmed pandemic influenza A (H1N1) virus infection in Turkey, May 15-November 30, 2009.
PMID: 20657062
2010
Japanese journal of infectious diseases
Abstract: There was no isolate harbored mutation at the position H275Y of the NA gene, indicating that the virus isolates currently circulating in Turkey are sensitive to oseltamivir.
Antiviral susceptibility of avian and swine influenza virus of the N1 neuraminidase subtype.
Abstract: Sequence analysis of the outliers did not detect molecular markers of drug-resistance (e.g., H275Y NA mutation [N1 numbering]) but revealed mutations outside the NA active site.