Multifunctional transmembrane protein that plays several key roles in viral replication. Rapidely traffics from the host endoplasmic reticulum to the outer mitochondrial membrane where it acts to inhibit host immune response, block apoptotic signaling, regulate calcium flux, and induce mitochondrial fragmentation. Sequesters proapoptotic BAX at the outer mitochondrial membrane and prevents cytochrome c release and subsequent initiation of the proapoptotic cascade. Also provoques a calcium efflux from host endoplasmic reticulum and F-actin cytoskeleton disruption. Participates in the increase of host mitochondrial biogenesis, thus promoting viral replication by efficient use of newly made mitochondria. Additionally, a subset of vMIA localizes to peroxisomes, causing fragmentation and blocking peroxisomal MAVS signaling. Mechanistically, inhibits host MAVS oligomerization at peroxisomes in a mitochondrial fission factors (MFF)-dependent manner and in mitochondria independently of mitochondrial fission factors. Plays an essential role in the trafficking of host viperin/RSAD2 from the endoplasmic reticulum to the viral assembly compartment via the mitochondria during viral infection as failure of viperin to localize to the mitochondria results in insufficient lipogenesis and thus reduces viral replication