ArticleAntimicrobial agents and chemotherapy2015
Characterization of a large cluster of influenza A(H1N1)pdm09 viruses cross-resistant to oseltamivir and peramivir during the 2013-2014 influenza season in Japan.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 81 citations in OpenAlex.
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- Epidemiological and genomic surveillance of influenza A virus (pdm09 H1N1 and H3N2) strains from 2017 to 2025 in Tianjin, China.Virologica Sinica · 2025Article
- Influenza A(H1N1)pdm09 Virus with Reduced Susceptibility to Baloxavir, Japan, 2024.Emerging infectious diseases · 2025Article
- An outbreak of influenza A(H1N1)pdm09 antigenic variants exhibiting cross-resistance to oseltamivir and peramivir in an elementary school in Japan, September 2024.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2024Article
- Loxapine inhibits replication of hepatitis A virus in vitro and in vivo by targeting viral protein 2C.PLoS pathogens · 2024Article
- Efficacy of favipiravir against influenza virus resistant to both baloxavir and neuraminidase inhibitors.The Journal of antimicrobial chemotherapy · 2023Article
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- Antiviral options and therapeutics against influenza: history, latest developments and future prospects.Frontiers in cellular and infection microbiology · 2023Review
- Population analysis of oseltamivir-resistant variants for the rapid prediction of drug susceptibility by real-time reverse transcription polymerase chain reaction.Fukushima journal of medical science · 2022Article
- Assessing the fitness of a dual-antiviral drug resistant human influenza virus in the ferret model.Communications biology · 2022Article
- Predicting Permissive Mutations That Improve the Fitness of A(H1N1)pdm09 Viruses Bearing the H275Y Neuraminidase Substitution.Journal of virology · 2022Article
- Global update on the susceptibilities of human influenza viruses to neuraminidase inhibitors and the cap-dependent endonuclease inhibitor baloxavir, 2018-2020.Antiviral research · 2022Review
- Antivirals Targeting the Neuraminidase.Cold Spring Harbor perspectives in medicine · 2022Review
- COVID-19, Influenza and RSV: Surveillance-informed prevention and treatment - Meeting report from an isirv-WHO virtual conference.Antiviral research · 2022Article
- Influenza polymerase inhibitor resistance: Assessment of the current state of the art - A report of the isirv Antiviral group.Antiviral research · 2021Review
- Article
- Evaluating the fitness of PA/I38T-substituted influenza A viruses with reduced baloxavir susceptibility in a competitive mixtures ferret model.PLoS pathogens · 2021Article
- Antivirals Targeting the Surface Glycoproteins of Influenza Virus: Mechanisms of Action and Resistance.Viruses · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Between September 2013 and July 2014, 2,482 influenza 2009 pandemic A(H1N1) [A(H1N1)pdm09] viruses were screened in Japan for the H275Y substitution in their neuraminidase (NA) protein, which confers cross-resistance to oseltamivir and peramivir. We found that a large cluster of the H275Y mutant virus was present prior to the main influenza season in Sapporo /: Hokkaido, with the detection rate for this mutant virus reaching 29% in this area. Phylogenetic analysis suggested the clonal expansion of a single mutant virus in Sapporo /: Hokkaido. To understand the reason for this large cluster, we examined the in vitro and in vivo properties of the mutant virus. We found that it grew well in cell culture, with growth comparable to that of the wild-type virus. The cluster virus also replicated well in the upper respiratory tract of ferrets and was transmitted efficiently between ferrets by way of respiratory droplets. Almost all recently circulating A(H1N1)pdm09 viruses, including the cluster virus, possessed two substitutions in NA, V241I and N369K, which are known to increase replication and transmission fitness. A structural analysis of NA predicted that a third substitution (N386K) in the NA of the cluster virus destabilized the mutant NA structure in the presence of the V241I and N369K substitutions. Our results suggest that the cluster virus retained viral fitness to spread among humans and, accordingly, caused the large cluster in Sapporo/Hokkaido. However, the mutant NA structure was less stable than that of the wild-type virus. Therefore, once the wild-type virus began to circulate in the community, the mutant virus could not compete and faded out.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.