Cell death signalling in virus infection

Apoptosis, necroptosis and pyroptosis represent three major regulated cell death modalities. Apoptosis features cell shrinkage, nuclear fragmentation and cytoplasm-blebbing. Necroptosis and pyroptosis exhibit osmotic imbalances in the cell accompanied by early membrane ruptures, which morphologically resembles necrosis. Importantly, these two lytic cell death forms facilitate the release of damage associated molecular patterns into the extracellular space leading to inflammatory response. Whereas, during apoptosis, the membrane integrity is preserved and the apoptotic cell is removed by neighbouring cells ensuring the avoidance of immune-stimulation. Viruses comprise a versatile group of intracellular pathogens, which elicit various strategies to infect and to propagate. Viruses are recognized by a myriad of pathogen recognition receptors in the human cells, which consequently lead to activation of the immune system and in certain circumstances cell-autonomous cell death. Importantly, the long-standing view that a cell death inducing capacity of a virus is equal to its pathogenic potential seems to be only partially valid. The altruistic cell death of an infected cell may serve the whole organism by ultimately curbing the way of virus manufacturing. In fact, several viruses express “anti-cell death” proteins to avoid this viral-defence mechanism. Conversely, some viruses hijack cell death pathways to selectively destroy cell populations in order to compromise the immune system of the host. This review discusses the pros and cons of virus induced cell death from the perspective of the host cells and attempts to provide a comprehensive overview of the complex network of cell death signalling in virus infection.