Mechanism of cell cycle regulation and cell proliferation during human viral infection.

Abstract

Over the history of the coevolution of Host viral interaction, viruses have customized the host cellular machinery into their use for viral genome replication, causing effective infection and ultimately aiming for survival. They do so by inducing subversions to the host cellular pathways like cell cycle via dysregulation of important cell cycle checkpoints by viral encoded proteins, arresting the cell cycle machinery, blocking cytokinesis as well as targeting subnuclear bodies, thus ultimately disorienting the cell proliferation. Both DNA and RNA viruses have been active participants in such manipulation resulting in serious outcomes of cancer. They achieve this by employing different mechanisms-Protein-protein interaction, protein-phosphorylation, degradation, redistribution, viral homolog, and viral regulation of APC at different stages of cell cycle events. Several DNA viruses cause the quiescent staged cells to undergo cell cycle which increases nucleotide pools logistically significantly persuading viral replication whereas few other viruses arrest a particular stage of cell cycle. This allows the latter group to sustain the infection which allows them to escape host immune response and support viral multiplication. Mechanical study of signaling such viral mediated pathways could give insight into understanding the etiology of tumorigenesis and progression. Overall this chapter highlights the possible strategies employed by DNA/RNA viral families which impact the normal cell cycle but facilitate viral infected cell replication. Such information could contribute to comprehending viral infection-associated disorders to further depth.