Viral-mediated activation and inhibition of programmed cell death

Viruses are ubiquitous intracellular genetic parasites that heavily rely on the infected cell to complete their replication life cycle. This dependency on the host machinery forces viruses to modulate a variety of cellular processes including cell survival and cell death. Viruses are known to activate and block almost all types of programmed cell death (PCD) known so far. Modulating PCD in infected hosts has a variety of direct and indirect effects on viral pathogenesis and antiviral immunity. The mechanisms leading to apoptosis following virus infection is widely studied, but several modalities of PCD, including necroptosis, pyroptosis, ferroptosis, and paraptosis, are relatively understudied. In this review, we cover the mechanisms by which viruses activate and inhibit PCDs and suggest perspectives on how these affect viral pathogenesis and immunity.

Automated summary

Viruses heavily rely on infected cells to replicate and modulate various cellular processes, including cell survival and cell death. They can activate and block different types of programmed cell death (PCD), which have direct and indirect effects on viral pathogenesis and antiviral immunity. While the mechanisms of apoptosis following virus infection have been widely studied, other forms of PCD, such as necroptosis, pyroptosis, ferroptosis, and paraptosis, are relatively understudied. This review covers the mechanisms by which viruses activate and inhibit PCDs and discusses their impact on viral pathogenesis and immunity.