The global pandemic of SARS-CoV-2 in the past 2 years has aroused great attention to infectious diseases, and emerging virus outbreaks have brought huge challenges to the global health system. Viruses are specific pathogens that completely rely on host cells for their own survival and disease transmission. At present, a growing number of studies have proved that inducing the death of virus-infected cells can prevent the spread of virus and promote disease recovery. Therefore, many ways to induce the death of infected cells are considered to be beneficial to host immunity. Cell death is a basic biological phenomenon. Programmed cell death (PCD), as an important part of the host's innate immune response, provides effective protection against virus transmission. Pyroptosis, apoptosis, and necroptosis are the most commonly studied pathways of PCD. Recent studies have found that three pathways of cell death can be activated during virus infection. More and more studies have shown the existence of extensive connections between PCDs, and this complex relationship is defined as PANoptosis, an inflammatory PCD pathway regulated by the PANoptosome complex, whose characteristics cannot be explained by any of the three PCD pathways. During viral infection, PANoptosis can promote inflammatory response by inducing the production of inflammatory cytokines and cell death to exert an antiviral mechanism. This article reviews the various effects of cell death pathways during viral infection and provides new ideas for clinical antiviral therapy and related immunotherapy.
Keywords: PANoptosis; apoptosis; cell death; necroptosis; programmed cell death; pyroptosis; virus.