Mechanisms by which Viral Proteins of Human DNA Tumor Viruses Hijack the Cell Cycle pp. 43-88
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Authors: (Mona Johannessen, Ugo Moens, University of Tromsų, Faculty of Medicine, Institute of Medical Biology, Department of Microbiology and Virology, Tromsų, Norway)
Abstract: Viruses are obligate intracellular parasites with a restricted genome size encoding a limited number of genes. To compensate for their small number of proteins, viruses often usurp cellular proteins to complete their life-cycle. Their propagation time in a permissive host cell is often very short and to speed up their replication, these viruses can subvert the host cell cycle. Despite their vast genetic diversity, DNA tumor viruses have evolved common mechanisms to disorder the cell cycle. Viral-encoded proteins can activate cellular proteins that allow the cell to enter the S phase or to arrest in the G2 phase. Moreover, viral proteins may initiate cell cycle progression by destroying the suppressive activity of tumor suppressors such as p53, the pRB family members, and cyclin-dependent protein kinase inhibitors. In addition, some of these viruses encode their own cyclins that allow them to steer cellular cyclin-dependent kinases. This review will focus on the different mechanisms by which human DNA tumor viruses hijack the cell cycle, and will discussed the application of cell cycle inhibitors as potential therapeutic against viral infections.
