Influenza a virus (iav) is responsible for yearly epidemics and sporadic pandemics. understanding the mechanism by which the inflammatory response is mounted and controlled is key to manage the disease. iav perturbs a variety of metabolic pathways including macroautophagy. macroautophagy, hereafter referred to as autophagy, is a catabolic pathway that is active in all nucleated cells. in stress condition, autophagic activity can be increased. a variety of viruses perturb autophagy. iav has been described to both induce autophagy and block its completion mainly through its matrix protein 2 (m2). however, the impact of such perturbation on viral replication and host cell response to infection is still unknown. i developed cellular models in which autophagy capacity can be specifically restored in cell lines that are otherwise autophagy-incompetent. using these models, i showed that autophagy does not impact iav infection and replication but inhibits interferon-β induction at early stages post infection, leading to dampened induction of interferon-stimulated genes. i showed that m2 does not prevent autophagy completion by itself but only in the context of iav in a caspase-activation dependent fashion. in summary, my thesis work, using these novel autophagy models, revealed that early autophagy induction post-iav infection inhibits ifn-β, leading to a global decrease in interferon stimulated gene expression. indeed, sustained autophagy perturbation through m2 may allow iav to limit the ifn-β response throughout its life cycle. preventing m2-mediated autophagy perturbation may allow us to develop new antiviral strategies as well as new live attenuated iav vaccines.