Influenza A virus is a dreadful pathogen of animals and humans, causing 
widespread infection and severe morbidity and mortality. It is essential to 
characterize the influenza A virus-host interaction and develop efficient 
counter measures against the viral infection. Autophagy is known as a catabolic 
process for the recycling of the cytoplasmic macromolecules. Recently, it has 
been shown that autophagy is a critical mechanism underlying the interaction 
between influenza A virus and its host. Autophagy can be induced by the 
infection with influenza A virus, which is considered as a necessary process for 
the viral proliferation, including the accumulation of viral elements during the 
replication of influenza A virus. On the other hand, influenza A virus can 
inhibit the autophagic formation via interaction with the autophagy-related 
genes (Atg) and signaling pathways. In addition, autophagy is involved in the 
influenza virus-regulated cell deaths, leading to significant changes in host 
apoptosis. Interestingly, the high pathogenic strains of influenza A virus, such 
as H5N1, stimulate autophagic cell death and appear to interplay with the 
autophagy in distinct ways as compared with low pathogenic strains. This review 
discusses the regulation of autophagy, an influenza A virus driven process.