Modeling Dysplastic and Functional Lung Alveolar Repair after Influenza Infection.

Abstract

Viral infection causes both acute and long-term damage to the lung alveolus, the specialized tissue structure responsible for gas exchange between the cardiovascular system and the external environment. Influenza A virus (IAV) infection in mice represents a translational model for the response of the human lung to viral infection and induces both transient and persistent cell state changes in the alveolus. In some cases, aberrant cell states induced by viral injury that are not resolved over time may permanently impair the critical gas exchange function of the lung. This article demonstrates methods for intranasal infection of mice with A/PR/8/34 IAV and characterization of transient and long-lasting alterations to the cellular composition and tissue structure of damaged lungs. This model enables a detailed investigation into the molecular and cellular mechanisms underlying lung repair and chronic dysfunction. This approach also offers a platform for evaluating therapeutic interventions aimed at promoting effective lung regeneration and restoring respiratory function after viral injury.