Initiation of cytomegalovirus infection at ND10.

As a large double-stranded DNA virus, CMV replicates in the nucleus, a highly structured environment. Diffusional and solid phases exist as interdependent sets of interactions between many components that determine either replicative success of an infecting virus or the defensive success of the host cell. In their extremes, cell death may be part of the lytic release of viral particles, or, in defense terms, the ultimate sacrifice preventing virus release. Between these extremes exists an evolutionarily derived standoff between virus and cell. Exogenous shifts in homeostasis can disturb this balance, diminishing the cell's defensive powers and reactivating the silenced viral genome. Many of the solid-phase aspects of this process can be seen in situ and analyzed. This review evaluates structural information derived from CMV-infected cells in situ at very early times of infection and the conceptional advances derived from them, mostly centering on the major immediate early gene products, specifically IE1. A scientific basis for considering the major immediate early proteins as potential targets in suppressing CMV disease is discussed.