ArticleJournal of virology2012
Incoming influenza A virus evades early host recognition, while influenza B virus induces interferon expression directly upon entry.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Hypertransaminasemia Is a Marker of Severity in Children Hospitalized for Influenza.Influenza and other respiratory viruses · 2026Article
- IFN-gene signatures in B cells following influenza A and B virus infection and influenza vaccination.EMBO molecular medicine · 2026Article
- Host-pathogen interaction in community-acquired pneumonia: a focus on the immune response.Frontiers in cellular and infection microbiology · 2026Review
- Differential interferon responses to influenza A and B viruses in primary ferret respiratory epithelial cells.Journal of virology · 2024Article
- Existing Evidence for Influenza B Virus Adaptations to Drive Replication in Humans as the Primary Host.Viruses · 2023Review
- The circRNA circVAMP3 restricts influenza A virus replication by interfering with NP and NS1 proteins.PLoS pathogens · 2023Article
- Article
- Epidemiological and Clinical Characteristics of Influenza Outbreaks Among Children in Chongqing, China.Frontiers in public health · 2022Article
- Library-based analysis reveals segment and length dependent characteristics of defective influenza genomes.PLoS pathogens · 2021Article
- SARS-CoV-2 Isolates Show Impaired Replication in Human Immune Cells but Differential Ability to Replicate and Induce Innate Immunity in Lung Epithelial Cells.Microbiology spectrum · 2021Article
- Cellular co-infection can modulate the efficiency of influenza A virus production and shape the interferon response.PLoS pathogens · 2020Article
- Cell type- and replication stage-specific influenza virus responses in vivo.PLoS pathogens · 2020Article
- Single cell heterogeneity in influenza A virus gene expression shapes the innate antiviral response to infection.PLoS pathogens · 2020Article
- Severity and outcomes of influenza-related pneumonia in type A and B strains in China, 2013-2019.Infectious diseases of poverty · 2020Article
- Influenza virus NS1- C/EBPβ gene regulatory complex inhibits RIG-I transcription.Antiviral research · 2020Article
- Next-Generation Sequencing Analysis of Cellular Response to Influenza B Virus Infection.Viruses · 2020Article
- The Development and Use of Reporter Influenza B Viruses.Viruses · 2019Review
- Cytoplasm and Beyond: Dynamic Innate Immune Sensing of Influenza A Virus by RIG-I.Journal of virology · 2019Review
- Inhibition of Ongoing Influenza A Virus Replication Reveals Different Mechanisms of RIG-I Activation.Journal of virology · 2019Article
- Comparative Outcomes of Adults Hospitalized With Seasonal Influenza A or B Virus Infection: Application of the 7-Category Ordinal Scale.Open forum infectious diseases · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of the interferon (IFN) system, which is triggered largely by the recognition of viral nucleic acids, is one of the most important host defense reactions against viral infections. Although influenza A and B viruses, which both have segmented negative-strand RNA genomes, share major structural similarities, they have evolutionarily diverged, with total genetic incompatibility. Here we compare antiviral-inducing mechanisms during infections with type A and B influenza viruses in human dendritic cells. We observed that IFN responses are induced significantly faster in cells infected with influenza B virus than in cells infected with type A influenza virus and that the early induction of antiviral gene expression is mediated by the activation of the transcription factor IFN regulatory factor 3 (IRF3). We further demonstrate that influenza A virus infection activates IFN responses only after viral RNA (vRNA) synthesis, whereas influenza B virus induces IFN responses even if its infectivity is destroyed by UV treatment. Thus, initial viral transcription, replication, and viral protein synthesis are dispensable for influenza B virus-induced antiviral responses. Moreover, vRNA molecules from both type A and B viruses are equally potent activators of IFN induction, but incoming influenza B virus structures are recognized directly in the cytosol, while influenza A virus is able to evade early recognition. Collectively, our data provide new evidence of a novel antiviral evasion strategy for influenza A virus without a contribution of the viral NS1 protein, and this opens up new insights into different influenza virus pathogenicities.
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