Final answer:
Adenoviruses trigger apoptosis in infected cells through DNA damage and mitochondrial cell death pathways, which, if happening early enough in the viral cycle, can prevent the release of infectious virions. Cytotoxic T cells and NK cells also contribute to this process through the use of fas ligand molecules and the release of perforin and granzymes.
Step-by-step explanation:
Adenoviruses have evolved mechanisms to induce apoptosis in infected cells, thereby preventing the proliferation of the virus. Although the specific pathways can vary, a significant mechanism through which adenoviruses induce apoptosis is by interfering with the infected cell's machinery, which may lead to DNA damage and activation of the mitochondrial cell death pathway. This can occur in a CD95/Fas receptor, FADD, and caspase-8-independent manner, indicating adenoviruses can trigger apoptosis without the direct activation of death receptors or the extrinsic apoptotic pathway.
In the context of immune response, cytotoxic T cells and NK cells contribute to the induction of apoptosis in virally infected cells. These cells interact with infected cells using fas ligand molecules that bind to fas receptors on the target cells, promoting apoptosis. Additionally, cytotoxic granules containing perforin and granzyme molecules released by these cells can penetrate the virally infected cell membranes, leading to apoptosis.
These apoptosis-inducing mechanisms are an important defense strategy, as they eliminate cells before the virus can complete its replication cycle, hence no infectious virions are released to further spread the infection.