Rapid replication of RNA viruses requires substantial cellular energy and effective mechanisms to evade cellular immunity. To meet these demands, many RNA viruses manipulate mitochondrial dynamics, including mitochondrial fragmentation and mitophagy. In the upcoming hypothesis, I propose a potential role for mitochondria-eating protein (MIEAP, also known as SPATA18), a novel regulator of non-canonical mitophagy, in the cellular pathogenesis and replication of H1N1 influenza v