Abstract: S247N is a novel, naturally occurring N1 neuraminidase mutation that reduces oseltamivir sensitivity and greatly potentiates oseltamivir resistance in the context of the H275Y mutation.
Abstract: Here we show that highly oseltamivir-resistant viruses containing both the S247N and H275Y mutations transmit efficiently in the guinea pig transmission model.
Recovery of influenza B virus with the H273Y point mutation in the neuraminidase active site from a human patient.
PMID: 22535992
2012
Journal of clinical microbiology
Abstract: The H275Y oseltamivir resistance mutation confers high-level resistance to oseltamivir in isolates of human A(H1N1) influenza.
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Abstract: More seriously, the efficacy of these two inhibitors against the double mutant I223R/H275Y (IRHY(2)) was significantly reduced by a factor of 12 374 and 21 times, respectively, compared to the wild-type.(2) This has led to the question of why the efficacy of the NA inhibitors is reduced by the occurrence of these mutations and, specifically, why the efficacy of oseltamivir against the double mutant IRHY was significantly reduced, to the point where oseltamivir has become an ineffective treatment.
Clinical effectiveness of neuraminidase inhibitors--oseltamivir, zanamivir, laninamivir, and peramivir--for treatment of influenza A(H3N2) and A(H1N1)pdm09 infection: an observational study in the 2010-2011 influenza season in Japan.
PMID: 22644080
2012
Journal of infection and chemotherapy
Abstract: Based on a cycling probe real-time polymerase chain reaction (PCR) assay, none of the A(H1N1)pdm09 strains in this study had the H275Y mutation conferring oseltamivir resistance.
Intrahost emergent dynamics of oseltamivir-resistant virus of pandemic influenza A (H1N1) 2009 in a fatally immunocompromised patient.
PMID: 22661221
2012
Journal of infection and chemotherapy
Abstract: By constructing minimum spanning trees, it is proposed that the H275Y mutant might be generated primarily in the nasopharynx, then spread to the right and left lungs.
Abstract: Here we detected the uneven distribution of H275Y mutant virus in a patient who received a 21-day long-term administration of oseltamivir.
Abstract: Intrahost variation of the virus showed that the H275Y mutant virus was the predominant population in both nasopharynx and right lung, whereas the oseltamivir-sensitive virus comprised half the population in the left lung.
Abstract: The oseltamivir-resistant pandemic influenza virus A (2009 H1N1) with H275Y mutation in neuraminidase (NA) has been sporadically reported, and its wide spread remains a potential threat.
Table:
Oseltamivir-resistant 2009 H1N1 influenza pneumonia during therapy in a renal transplant recipient.
Abstract: Ongoing surveillance is essential to monitor how oseltamivir-resistant H275Y mutant viruses may evolve in the future.
Abstract: The emergence of oseltamivir-resistant 2009 H1N1 influenza virus (conferred by the H275Y substitution in NA) during therapy or prophylaxis in immunocompromised patients is a serious concern.
Treatment of oseltamivir-resistant influenza A (H1N1) virus infections in mice with antiviral agents.
Abstract: Influenza A/Mississippi/03/2001 (H1N1) and A/Hong Kong/2369/2009 (H1N1) viruses containing the neuraminidase gene mutation H275Y (conferring resistance to oseltamivir) were adapted to mice and evaluated for suitability as models for lethal infection and antiviral treatment.
Method: Influenza A/HK-H275Y virus was provided by Kwok-Yung Yuen, The University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China.
Method: Influenza A/MS-H275Y was obtained from the Neuraminidase Inhibitor Surveillance Network (Melbourne, Australia).
Method: The mouse-adapted viruses were partially se
Discussion: Amantadine's 100% protective activity at the highest dose against the A/MS-H275Y virus infection was similar to that seen previously.
Identification of a Permissive Secondary Mutation That Restores the Enzymatic Activity of Oseltamivir Resistance Mutation H275Y.
Abstract: A parallel analysis of the H275Y mutation in the prior seasonal A/Brisbane/59/2007 background shows similar changes in the infection kinetic parameters, but in this background, the H275Y mutation also allows the mutant to infect cells five times more rapidly.
Abstract: The H275Y amino acid substitution of the neuraminidase gene is the most common mutation conferring oseltamivir resistance in the N1 subtype of the influenza virus.
Abstract: Using a mathematical model to analyze a set of in vitro experiments that allow for the full characterization of the viral replication cycle, we show that the primary effects of the H275Y substitution on the pandemic H1N1 (H1N1pdm09) strain are to lengthen the mean eclipse phase of infected cells (from 6.6 to 9.1 h) and decrease (by 7-fold) the viral burst size, i.e
H1N1 2009 pandemic influenza virus: resistance of the I223R neuraminidase mutant explained by kinetic and structural analysis.
Abstract: To understand the resistance mechanism of this mutation, the enzymatic properties of the I223R mutant, together with the most frequently observed resistance mutation, H275Y, and the double mutant I223R/H275Y were compared.
Introduction: Both I223R and H275Y changes are near the active site of A/H1N1 pandemic NA.
Introduction: Both in vitro studies and in animal models, viruses with I223R and the combination of I223R with H275Y were found not to be compromised in their replication capacity or transmissibility.
Introduction: Here we address the role of the I223R in
[National Influenza Surveillance Programme: results of influenza activity in Portugal in the 2010/2011 season].
Abstract: To date, the LNRVG detected the presence of the H275Y substitution in the neuraminidase gene, associated with oseltamivir resistance, in three virus A(H1)pdm09.For one of them, oseltamivir resistance was confirmed by phenotypic assays.
IV mutation literature information.
PMID: 
2012
Journal of virology
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