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Respiratory viruses are triggers of approximately half of all acute exacerbations of chronic obstructive pulmonary disease (AE-COPD).1–3 Such exacerbations are pivotal events that accelerate lung function decline, drive substantial morbidity and result in major healthcare expenditure. Rhinoviruses and influenza are among the most frequently detected pathogens, but it is increasingly recognised that different viruses can exhibit distinct exacerbation patterns.4–6 To date, rhinovirus-driven pathways have been extensively characterised, aided by innovative human challenge models.7 In contrast, epithelial-intrinsic mechanisms linking influenza infection to immune dysregulation have received comparatively less attention. Influenza-induced COPD exacerbations may often be associated with requirement for respiratory support, critical care admission and mortality, underscoring the need to better understand intrinsic virus-specific mechanisms.5 8