ArticleDevelopmental and comparative immunology2017
The NS1 protein of H5N6 feline influenza virus inhibits feline beta interferon response by preventing NF-κB and IRF3 activation.
Article in Developmental and comparative immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Avian Influenza Virus Infections in Felines: A Systematic Review of Two Decades of Literature.Open forum infectious diseases · 2025Review
- Molecular Markers and Mechanisms of Influenza A Virus Cross-Species Transmission and New Host Adaptation.Viruses · 2024Review
- Molecular characterization and antiviral effects of canine interferon regulatory factor 1 (CaIRF1).BMC veterinary research · 2022Article
- Canine Circovirus Suppresses the Type I Interferon Response and Protein Expression but Promotes CPV-2 Replication.International journal of molecular sciences · 2022Article
- Integrated Lung and Tracheal mRNA-Seq and miRNA-Seq Analysis of Dogs with an Avian-Like H5N1 Canine Influenza Virus Infection.Frontiers in microbiology · 2018Article
- The Drivers of Pathology in Zoonotic Avian Influenza: The Interplay Between Host and Pathogen.Frontiers in immunology · 2018Review
- Avian influenza overview October 2016-August 2017.EFSA journal. European Food Safety Authority · 2017Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the apparent lack of a feline influenza virus lineage, cats are susceptible to infection by influenza A viruses. Here, we characterized in vitro A/feline/Guangdong/1/2015, an H5N6 avian influenza virus recently isolated from cats. A/feline/Guangdong/1/2015 replicated to high titers and caused CPE in feline kidney cells. We determined that infection with A/feline/Guangdong/1/2015 did not activate the IFN-β promoter, but inhibited it by blocking the activation of NF-κB and IRF3. We also determined that the viral NS1 protein mediated the block, and that the dsRNA binding domain of NS1 was essential to perform this function. In contrast to treatment after infection, cells pretreated with IFN-β suppressed viral replication. Our findings provide an example of an H5N6 influenza virus suppressing IFN production, which might be associated with interspecies transmission of avian influenza viruses to cats.
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