IFNγ-Driven Inflammatory Responses in the Nasal Mucosa Drive Influenza Virus Shedding and Transmission

2026 · doi:10.64898/2026.01.06.698034
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Influenza A virus H3 hemagglutinin drives increased shedding and transmission through interferon gamma-induced nasal mucosal inflammation and mucus hypersecretion.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-14 · read from full text ⓘ

The study examined what drives host infectiousness during influenza A infection using an infant mouse model of viral transmission, comparing H3-containing and non-H3-containing influenza viruses with similar upper respiratory tract (URT) replication. H3 infection led to greater URT inflammation, including increased cytokine production, immune cell recruitment, mucus hypersecretion, and transcriptomic enrichment of interferon-stimulated gene programs dominated by an interferon gamma (IFNγ) signature, which correlated with viral shedding efficiency. Functional experiments showed that IFNγ deficiency reduced mucus production, shedding, and transmission, while IFNγ supplementation restored these outcomes. The paper does not evaluate whether these findings generalize beyond this infant mouse transmission model or beyond the specific H3 versus non-H3 comparison. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

What determines host infectiousness during influenza A virus (IAV) infection remains a fundamental unanswered question in virology. While upper respiratory tract (URT) replication is necessary for transmission, it’s insufficient to explain host-to-host variation in contagiousness. Using the infant mouse model of influenza transmission, we show that viruses containing H3 hemagglutinin shed at higher levels than non-H3-containing viruses, despite comparable URT replication. H3-containing virus infection was associated with higher URT inflammation, characterized by increased cytokine production, immune cell recruitment, and mucus hypersecretion, which directly correlated with shedding efficiency. Transcriptomic profiling identified enrichment of interferon-stimulated gene programs, with a dominant interferon gamma (IFNγ) signature during H3 infections. Functional studies demonstrated that IFNγ deficiency reduced mucus production, shedding, and transmission, whereas IFNγ supplementation restored these phenotypes. Together, these findings identify IFNγ-driven mucosal inflammation key host determinant of influenza infectiousness, reframing contagiousness as a consequence of host inflammatory clearance rather than viral replication alone.
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Abstract What determines host infectiousness during influenza A virus (IAV) infection remains a fundamental unanswered question in virology. While upper respiratory tract (URT) replication is necessary for transmission, it’s insufficient to explain host-to-host variation in contagiousness. Using the infant mouse model of influenza transmission, we show that viruses containing H3 hemagglutinin shed at higher levels than non-H3-containing viruses, despite comparable URT replication. H3-containing virus infection was associated with higher URT inflammation, characterized by increased cytokine production, immune cell recruitment, and mucus hypersecretion, which directly correlated with shedding efficiency. Transcriptomic profiling identified enrichment of interferon-stimulated gene programs, with a dominant interferon gamma (IFNγ) signature during H3 infections. Functional studies demonstrated that IFNγ deficiency reduced mucus production, shedding, and transmission, whereas IFNγ supplementation restored these phenotypes. Together, these findings identify IFNγ-driven mucosal inflammation key host determinant of influenza infectiousness, reframing contagiousness as a consequence of host inflammatory clearance rather than viral replication alone. Competing Interest Statement The authors have declared no competing interest.

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