ArticleThe Journal of infectious diseases2015
Characterization of drug-resistant influenza A(H7N9) variants isolated from an oseltamivir-treated patient in Taiwan.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Virus-induced pathogenesis, vaccine development, and diagnosis of novel H7N9 avian influenza A virus in humans: a systemic literature review.The Journal of international medical research · 2020Pooled it
- Oseltamivir Resistance in Human Influenza A(H5N1) and A(H7N9) Infections: A Mini Review.Open forum infectious diseases · 2026Review
- Ceramide synthase 4 interferes with replication of influenza virus but is downregulated by infection.Journal of virology · 2025Article
- SREBP2-dependent lipid droplet formation enhances viral replication and deteriorates lung injury in mice following IAV infection.Emerging microbes & infections · 2025Article
- UiO-66 nanoparticles combat influenza A virus in mice by activating the RIG-I-like receptor signaling pathway.Journal of nanobiotechnology · 2024Article
- Melatonin alleviates lung injury in H1N1-infected mice by mast cell inactivation and cytokine storm suppression.PLoS pathogens · 2023Article
- Antiviral options and therapeutics against influenza: history, latest developments and future prospects.Frontiers in cellular and infection microbiology · 2023Review
- In Silico Studies Reveal Peramivir and Zanamivir as an Optimal Drug Treatment Even If H7N9 Avian Type Influenza Virus Acquires Further Resistance.Molecules (Basel, Switzerland) · 2022Article
- Substitution of I222L-E119V in neuraminidase from highly pathogenic avian influenza H7N9 virus exhibited synergistic resistance effect to oseltamivir in mice.Scientific reports · 2021Article
- Influenza A virus NS1 induces degradation of sphingosine 1-phosphate lyase to obstruct the host innate immune response.Virology · 2021Article
- Antiviral Activity of 3D, a Butene Lactone Derivative Against Influenza A Virus In Vitro and In Vivo.Viruses · 2021Article
- Article
- Functional neuraminidase inhibitor resistance motifs in avian influenza A(H5Nx) viruses.Antiviral research · 2020Article
- Selective and ATP-competitive kinesin KIF18A inhibitor suppresses the replication of influenza A virus.Journal of cellular and molecular medicine · 2020Article
- Research progress on human infection with avian influenza H7N9.Frontiers of medicine · 2020Review
- Pre-Treatment with Zirconia Nanoparticles Reduces Inflammation Induced by the Pathogenic H5N1 Influenza Virus.International journal of nanomedicine · 2020Article
- Novel Avian Influenza A Virus Infections of Humans.Infectious disease clinics of North America · 2019Review
- Inventory of molecular markers affecting biological characteristics of avian influenza A viruses.Virus genes · 2019Review
- Detection of oseltamivir-resistant zoonotic and animal influenza A viruses using the rapid influenza antiviral resistance test.Influenza and other respiratory viruses · 2019Article
- Inhibition of avian-origin influenza A(H7N9) virus by the novel cap-dependent endonuclease inhibitor baloxavir marboxil.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
backgroundPatients contracting influenza A(H7N9) infection often developed severe disease causing respiratory failure. Neuraminidase (NA) inhibitors (NAIs) are the primary option for treatment, but information on drug-resistance markers for influenza A(H7N9) is limited.
methodsFour NA variants of A/Taiwan/1/2013(H7N9) virus containing a single substitution (NA-E119V, NA-I222K, NA-I222R, or NA-R292K) recovered from an oseltamivir-treated patient were tested for NAI susceptibility in vitro; their replicative fitness was evaluated in cell culture, mice, and ferrets.
resultsNA-R292K led to highly reduced inhibition by oseltamivir and peramivir, while NA-E119V, NA-I222K, and NA-I222R caused reduced inhibition by oseltamivir. Mice infected with any virus showed severe clinical signs with high mortality rates. NA-I222K virus was the most virulent in mice, whereas virus lacking NA change (NA-WT) and NA-R292K virus seemed the least virulent. Sequence analysis suggests that PB2-S714N increased virulence of NA-I222K virus in mice; NS1-K126R, alone or in combination with PB2-V227M, produced contrasting effects in NA-WT and NA-R292K viruses. In ferrets, all viruses replicated to high titers in the upper respiratory tract but produced only mild illness. NA-R292K virus, showed reduced replicative fitness in this animal model.
conclusionsOur data highlight challenges in assessment of the replicative fitness of H7N9 NA variants that emerged in NAI-treated patients.
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