Moving the furniture around – how herpes simplex virus 1 remodels the host nucleus

Herpes simplex virus 1 (HSV-1) is a nuclear-replicating DNA virus that remodels the host cell nucleus to support viral gene expression, genome replication, and production of infectious progeny. During infection, HSV-1 alters chromatin organization, nuclear biophysical properties, and nuclear bodies composition and dynamics. These changes reflect viral strategies to counteract intrinsic anti-viral defenses and reorgenaize host nuclear functions to favor infection. Viral replication compartments reshape the nuclear environment and interact with nuclear bodies involved in RNA metabolism and gene regulation. HSV-1 mRNAs, many of which are intronless, rely on host export pathways adapted by viral factors such as ICP27, which links viral transcripts to host export receptors including NXF1. Recent evidence suggests that nuclear speckles may serve as specialized intranuclearhubs for immediate-early viral transcripts before export. This review discusses how HSV-1 reorganizes nuclear architecture and nuclear bodies, to regulate viral gene expression, RNA processing and nuclear export.