Ontology highlight
ABSTRACT:
PROVIDER: PRJNA553555 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9661180.fastq.gz | Fastqsanger.gz | |||
| SRR9661190.fastq.gz | Fastqsanger.gz | |||
| SRR9661181.fastq.gz | Fastqsanger.gz | |||
| SRR9661191.fastq.gz | Fastqsanger.gz | |||
| SRR9661182.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to identify how the occupancy of RNA polymerase II (Pol II) on the host genome changes during HSV-1 infection and is impacted by the viral immediate early protein ICP4. Pol II ChIP-seq experiments after infection with the wild-type (WT) virus and mutant ICP4 (n12) virus, compared to mock infection, revealed global increases and decreases in Pol II occupancy on the host genome that depended upon ICP4.
2021-07-07 | GSE171600 | GEO
Project description:G-quadruplexes (G4s) are four-stranded nucleic acid structures abundant at gene promoters. They can adopt several distinctive conformations. G4s have been shown to form in the herpes simplex virus-1 (HSV-1) genome during its viral cycle. Here by cross-linking/pull-down assay we identified ICP4, the major HSV-1 transcription factor, as the protein that most efficiently interacts with viral G4s during infection. ICP4 specific and direct binding and unfolding of parallel G4s, including those present in HSV-1 immediate early gene promoters, induced transcription in vitro and in infected cells. This mechanism was also exploited by ICP4 to promote its own transcription. Proximity ligation assay allowed visualization of G4-protein interaction at the single selected G4 in cells. G4 ligands inhibited ICP4 binding to G4s. Our results indicate the existence of a well-defined G4-viral protein network that regulates the productive HSV-1 cycle. They also point to G4s as elements that recruit transcription factors to activate transcription in cells.
2021-09-10 | PXD024743 | Pride
Project description:The abundance of HSV mRNAs was determines over 16h of infection in wt (KOS) and n199 (ICP22 mutant) infected cells. ICP22 is an immediate early gene of HSV that affects gene expression
2018-01-20 | GSE109420 | GEO
Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.
2012-02-21 | E-GEOD-35943 | biostudies-arrayexpress
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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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.
2023-09-05 | GSE235226 | GEO
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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