Figure 3.

Three theoretical scenarios regarding lung epithelial cell apoptosis during pneumovirus infection, which may co-exist. First (A), viral infection triggers the mitochondrial (intrinsic) apoptotic pathway via interaction with Bcl-2 family proteins. Second (B), death receptor ligands (either membrane-bound or soluble) presented or secreted by local immune cells activate the death receptor (extrinsic) apoptotic pathway in viral-infected cells. Similarly, granzymes released from effector lymphocytes into the cytosol of target cells induce apoptosis. Viral infection may modulate the susceptibility to death receptor ligands or granzymes by altering the expression of and interaction with the protein machinery, such as surface death receptors, involved in these pathways. Third (C), bystander (uninfected) epithelial cells undergo apoptosis as a result of extensive, non-specific signaling via the death receptor (extrinsic) and/or granzyme apoptotic pathway.