HSV-1 ICP22 condensates impair host transcription by depleting promoter RNAPII Ser-2P occupation.

ABSTRACT: Herpes simplex virus type I (HSV-1) infection-induced host transcript ion shutdown is one of the most critical hallmarks of viral lytic infection. However, how HSV-1 and which viral factors accomplish this dramatic effect is not well understood. In this study, we show that ICP22-defined condensates shutdown host global transcription but facilitate viral transcription. This is independent of its effects on viral infection-triggered changes in splicing, readthrough, and read-in events. ICP22 condensates depleted the serine-2 phosphorylated RNA polymerase II (RNAPII Ser-2P) occupancy from the host transcription start site (TSS), resulting in decreased host transcripts output. At the same time, it ensures proper RNAPII Ser-2P distribution on the viral genome to promote viral transcription. Thi

SUBMITTER: Qi H 

PROVIDER: S-EPMC11876393 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature