Protein PB1-F2 PB1 PB1F2_I96A0 90 MEQEQDTPWTQSTEHINIQKRGNGQRTQRLEHPNSIRLMDHYLRIMSRVGMHKQIVYWKQWLSLKNPTQGSLKTRVLKRWKLFSKQEWIS 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. 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. May also act in trans: extracellular PB1-F2 released by infected cells could potentially inactivate hosts cell recruitment to the site of infection. During early stage of infection, may predispose the mitochondria to permeability transition through interaction with human 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 (By similarity).