Ontology highlight
ABSTRACT:
PROVIDER: PRJNA664709 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12681900.fastq.gz | Fastqsanger.gz | |||
| SRR12682000.fastq.gz | Fastqsanger.gz | |||
| SRR12681901.fastq.gz | Fastqsanger.gz | |||
| SRR12682001.fastq.gz | Fastqsanger.gz | |||
| SRR12681902.fastq.gz | Fastqsanger.gz |
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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.
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