Speckles and paraspeckles coordinate to regulate HSV-1 genes transcription

Li & Wang report that components of nuclear speckles and paraspeckles are redistributed upon HSV-1 infection. They show that the association of Serine/arginine-rich splicing factor 2 (SRSF2) with nuclear paraspeckles assembly transcript 1 (NEAT1) coordinates the transcription of viral genes Numbers of nuclear speckles and paraspeckles components have been demonstrated to regulate herpes simplex virus 1 (HSV-1) replication. However, how HSV-1 infection affects the two nuclear bodies, and whether this influence facilitates the expression of viral genes, remains elusive. In the current study, we found that HSV-1 infection leads to a redistribution of speckles and paraspeckles components. Serine/arginine-rich splicing factor 2 (SRSF2), the core component of speckles, was associated with multiple paraspeckles components, including nuclear paraspeckles assembly transcript 1 (NEAT1), PSPC1, and P54nrb, in HSV-1 infected cells. This association coordinates the transcription of viral genes by binding to the promoters of these genes. By association with the enhancer of zeste homolog 2 (EZH2) and P300/CBP complex, NEAT1 and SRSF2 influenced the histone modifications located near viral genes. This study elucidates the interplay between speckles and paraspeckles following HSV-1 infection and provides insight into the mechanisms by which HSV-1 utilizes host cellular nuclear bodies to facilitate its life cycle.

Automated summary

The study reveals that HSV-1 infection causes redistribution of nuclear speckles and paraspeckles components, which play a crucial role in regulating viral gene transcription by binding to specific gene promoters. This interaction influences histone modifications near viral genes, shedding light on how HSV-1 utilizes host cellular nuclear bodies to facilitate its life cycle.