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Effect of Cyclohexidmide treatment on early transcription of HSV-1 ΔICP22 and repaired virus

ABSTRACT: Study was performed to assess the requirement for HSV-1 IE protein, ICP22, to be expressed to regulate early HSV-1 transcription

ORGANISM(S): Homo sapiens

PROVIDER: GSE213098 | GEO | 2022/10/18

REPOSITORIES: GEO

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Immediate early proteins of herpes simplex virus transiently repress viral transcription before subsequent activation.

Project description:This study was undertaken to further clarify the roles of HSV-1 immediately early (IE) genes ICP4, ICP0, and ICP22 in early viral transcription. Precision nuclear Run On followed by deep Sequencing (PRO-Seq) was used to identify sites of Pol activity to high resolution on the genomes of HSV-1 viruses bearing mutations in a0, a4 or a22/US1, and corresponding viruses in which these loci were genetically restored. The results indicated that prior to initiating activation of transcription, IE genes first mediate transcriptional repression.

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Transcriptomic analysis of early HSV-1 transcription in the absence of the immediate early protein, ICP4 [PROSeq]

Project description:Herpes simplex virus 1 (HSV-1) transcription is tightly regulated in a temporal cascade, utilizing cellular RNA polymerase (Pol). We previously observed that infection with HSV-1 mutants lacking immediate early (IE) genes a0, a4 and a22 exhibited unusually high levels of aberrant transcription across the viral genome at just 1.5 hpi. The strongest effect occurred in the absence of a4, which is both an essential transcriptional activator and repressor. The goal of the current study was to define the mechanism of ICP4-mediated early transcriptional repression on the viral genome. Using the transcriptomic tools PRO-Cap, PRO-Seq, GRO-Seq and Nanopore direct RNA sequencing we found that initiation was elevated at viral promoters of all temporal classes in the absence of ICP4. Despite higher levels of initiation, transcription of non-IE genes was stalled within gene bodies and did not lead to production of mature mRNA. We therefore posit that HSV-1 retains additional ICP4-independent mechanisms to limit expression of viral genes that initiate prematurely. The data also indicated rapid release from promoter proximal pausing and progression along HSV IE genes and revealed termination as an important rate -limiting regulatory step. These findings highlight multiple mechanisms that HSV-1 employs to regulate early transcription and identify ICP4’s repressive role is to restrict initiation on non IE genes, thereby ensuring correct progression of the temporal cascade.

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq I)

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2023-06-20 | GSE185234 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (Omni-ATAC-seq III)

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