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Researchers have unveiled novel and unexpected methods through which human lung cells detect influenza virus and viral RNA, with potential therapeutic implications. Influenza viruses pose an annual threat to human health, causing epidemics affecting millions and resulting in significant fatalities. These viruses can induce severe symptoms in various populations, including the young, elderly, and immunocompromised individuals. Their primary target for replication is respiratory epithelial cells, where they inflict damage and cell death.
Contrary to earlier beliefs, scientists now recognize the pivotal role played by these epithelial cells in initiating the immune system’s antiviral response. They are not merely passive barriers; rather, they actively contribute to defense. The research team identified two distinct molecular pathways stimulated by viral RNA and influenza viruses. Specific proteins within these pathways trigger cascading reactions that culminate in the formation of membrane pores in the epithelial cells, known as “gasdermin D” and “gasdermin E.” These pores facilitate the release of specialized cytokines, activating the immune system and simultaneously causing cell death, thereby preventing viral spread.
To assess the significance of this discovery, the researchers suppressed the formation of gasdermin pores, resulting in increased influenza virus replication. This underscores the crucial role of gasdermins in the antiviral response. The findings have been published in the journal iScience. Professor Bowie, based in Trinity’s Biomedical Sciences Institute, emphasized the collaborative effort of an EU-wide network of scientists with expertise in immunology and virology. Their research sheds light on the initial response to viruses when the lungs first encounter them. This newfound knowledge not only advances our understanding of the immune response to influenza but also provides insights that may be relevant to other viral lung infections, such as SARS-CoV-2 and RSV.
