Plays an important role in promoting lung pathology in both primary viral infection and secondary bacterial infection. Promotes alteration of mitochondrial morphology, dissipation of mitochondrial membrane potential, and cell death. Alternatively, inhibits the production of interferon in the infected cell at the level of host mitochondrial antiviral signaling MAVS. Its level of expression differs greatly depending on which cell type is infected, in a manner that is independent of the levels of expression of other viral proteins. Monocytic cells are more affected than epithelial cells. Seems to disable virus-infected monocytes or other host innate immune cells. During early stage of infection, predisposes the mitochondria to permeability transition through interaction with host SLC25A6/ANT3 and VDAC1. These proteins participate in the formation of the permeability transition pore complex (PTPC) responsible of the release of mitochondrial products that triggers apoptosis. Oligomer. Interacts with human SLC25A6/ANT3 and VDAC1. Interacts with host MAVS. Inner mitochondrial membrane in most cells types. Otherwise is detected in the nucleus and cytosol. Is not encoded in all strains, and seems to be dispensable for replication. Belongs to the influenza viruses PB1-F2 family.