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Inflammatory, transcriptomic and cell fate responses underlying the mammalian transmission of avian influenza viruses, bulk RNAseq.

ABSTRACT: Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes. AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.

ORGANISM(S): Mustela putorius furo

PROVIDER: GSE296526 | GEO | 2025/07/28

REPOSITORIES: GEO

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Inflammatory, transcriptomic and cell fate responses underlying the mammalian transmission of avian influenza viruses

Project description:Airborne transmissibility of avian influenza viruses (AIVs) in humans is considered an essential component to their pandemic risk. While several viral factors regulating airborne transmission (AT) have been delineated, it is not known what, if any, responses at the respiratory epithelia are determinant of AIV AT. Using responses in the ferret nasal epithelium to a panel of H1N1 AIVs, here we describe host responses that segregate with AT phenotypes (DE300 and DE256 were AT and DE558 and DE213 were not AT). AIV infection upregulated interferon alpha and gamma responses, IL-6 JAK-STAT signaling and downregulated oxidative phosphorylation. Single cell transcriptomics revealed that cellular genotoxic stress, NF-kB, interferon and cell fate pathways differentiated host responses to AIVs with different transmissibility. These responses culminated in greater AIV antigen-containing exudate and debris in the respiratory spaces of the nasal epithelium of ferrets inoculated with AT AIVs. More abundant CMPK2, SP100 and CXCL10 transcription in infected epithelia were a hallmark of AT viruses. Overall, our study reveals host responses associated with AIV infection and transmission in the nasal epithelium, the determinant anatomical site of influenza virus transmission.

2025-07-28 | GSE298058 | GEO

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Project description:All respiratory viruses establish primary infections in the nasal epithelium, where efficient innate immune induction may prevent dissemination to the lower airway and thus minimize pathogenesis. Human coronaviruses (HCoVs) cause a range of pathologies, but the host and viral determinants of disease during common cold versus lethal HCoV infections are poorly understood. We model the initial site of infection using primary nasal epithelial cells cultured at air-liquid interface (ALI). HCoV-229E, HCoV-NL63 and human rhinovirus-16 are common cold-associated viruses that exhibit unique features in this model: early induction of antiviral interferon (IFN) signaling, IFN-mediated viral clearance, and preferential replication at nasal airway temperature (33ºC) which confers muted host IFN responses. In contrast, lethal SARS-CoV-2 and MERS-CoV encode antagonist proteins that prevent IFN-mediated clearance in nasal cultures. Our study identifies features shared among common cold-associated viruses, highlighting nasal innate immune responses as predictive of infection outcomes and nasally-directed IFNs as potential therapeutics.

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