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When a virus infects a cell, it must contend with a hostile environment and host machinery that is intrinsically antiviral. One of the hallmarks of herpes simplex virus (HSV) infection is the dramatic reorganization of the infected cell nucleus leading to the formation of large globular replication compartments in which gene expression, DNA replication, and encapsidation occur ([1], [2] and references therein) (see Figure 1). During infection, cellular factors that are beneficial to the virus are hijacked while other factors and pathways are degraded or inactivated. Two of the cellular homeostatic pathways affected by HSV-1 infection are the protein quality control (PQC) and DNA damage response pathways. These events are orchestrated by several viral proteins including the immediate early proteins ICP4, ICP27, ICP0, and ICP22 that allow the virus to create an environment conducive to infection and counteract the cell's intrinsic capacity to inhibit viral infection [3]–[6]. ICP4 and ICP27 play essential roles in stimulation of robust viral gene expression [3], [4]. The immediate early protein ICP0 activates viral and cellular gene expression and functions as an E3 ubiquitin ligase by degrading several cellular proteins [5], [7]. One target of ICP0 is PML, a major component of nuclear foci called ND10 that play a repressive role in viral gene expression. ICP0 interferes with several intrinsic host defense mechanisms including host interferon responses [5], [7], [8], thereby playing a major role in the establishment of a permissive viral infection. ICP22 is required for efficient growth and expression of late viral genes in some but not all cultured cells [6]. ICP22 also plays a role in the post-translational modification of the cellular RNA polymerase II ([9] and references therein). As described below, these immediate early proteins play important roles in remodeling the infected cell nucleus, hijacking host PQC machinery, and manipulating cellular DNA damage responses.    Figure 1  Hsc70 is detected in virus-induced chaperone-enriched (VICE) domains that form adjacent to replication compartments in HSV-1-infected cells.

Herpes Simplex Virus Reorganizes the Cellular DNA Repair and Protein Quality Control Machinery