To replicate their genomes in cells and generate new progeny, viruses typically require
factors provided by the cells that they have infected. Subversion of the cellular
machinery that controls replication of the infected host cell is a common activity
of many viruses. Viruses employ different strategies to deregulate cell cycle checkpoint
controls and modulate cell proliferation pathways. A number of DNA and RNA viruses
encode proteins that target critical cell cycle regulators to achieve cellular conditions
that are beneficial for viral replication. Many DNA viruses induce quiescent cells
to enter the cell cycle; this is thought to increase pools of deoxynucleotides and
thus, facilitate viral replication. In contrast, some viruses can arrest cells in
a particular phase of the cell cycle that is favorable for replication of the specific
virus. Cell cycle arrest may inhibit early cell death of infected cells, allow the
cells to evade immune defenses, or help promote virus assembly. Although beneficial
for the viral life cycle, virus-mediated alterations in normal cell cycle control
mechanisms could have detrimental effects on cellular physiology and may ultimately
contribute to pathologies associated with the viral infection, including cell transformation
and cancer progression and maintenance. In this chapter, we summarize various strategies
employed by DNA and RNA viruses to modulate the replication cycle of the virus-infected
cell. When known, we describe how these virus-associated effects influence replication
of the virus and contribute to diseases associated with infection by that specific
virus.