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Effects of host miR-138 on herpes simplex virus 1 gene expression in Neuro-2a cells and their dependence of the binding sites on ICP0 mRNA

ABSTRACT: We previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. Therefore we conducted this RNAseq experiment to assess the effects of miR-138 on expression of each individual viral gene to search for other viral targets of miR-138

ORGANISM(S): Mus musculus Human alphaherpesvirus 1

PROVIDER: GSE127501 | GEO | 2020/04/27

REPOSITORIES: GEO

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Identification of targets of miR-138 in Neuro-2a and 293T cells by RNAseq

Project description:We previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. We did not find other confirmed viral targets of miR-138. Therefore we conducted these RNAseq experiments (in combination with PAR-CLIP experiments whose results are uploaded separately) to identify host targets of miR-138 in two cell lines to explain the ICP0-independent effects on HSV-1 gene expression.

2020-04-27 | GSE127502 | GEO

Identification of viral and host targets of miR-138 by PAR-CLIP analysis of herpes simplex virus 2 infected 293T cells

Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.

2021-11-01 | GSE155402 | GEO

Identification of herpes simplex virus 1 and host targets of miR-138 by comparative PAR-CLIP in Neuro-2a and 293T cells

Project description:This is a part of the study that shows that a host microRNA, miR-138, represses herpes simplex virus 1 (HSV-1) gene expression through both viral and host targets. These PAR-CLIP analyses identified viral and host targets of miR-138 in Neuro-2a (mouse neuroblastoma) and 293T (human embryonic kidney) cells. We constructed two cell lines derived from Neuro-2a cells, one overexpressing miR-138 (N2A138) and one antagonizing miR-138 (N2Aanti138). We also constructed two cell lines derived from 293T cells, one overexpressing miR-138 (293T138) and one control cells (293Tcontrol). Uninfected N2A138 and N2Aanti138 were compared by PAR-CLIP for host targets in Neuro-2A cells. 293T138 and 293Tcontrol cells infected for 4 and 8 hours were compared by PAR-CLIP for HSV-1 targets in 293T cells. 293T138 and 293Tcontrol cells infected for 4 hours were also compared for host targets in 293T cells.

2020-04-27 | GSE127503 | GEO

Multifaceted roles of RAP80 during the Herpes simplex virus 1 life cycle

Project description:Herpes simplex virus 1 (HSV-1) is a widespread human pathogen that establishes lifelong infections, but understanding precise activity at each infection stage remains challenging. HSV-1 utilizes ubiquitination pathways to modulate cellular factors to facilitate its replication cycle, however, elucidating the cascades that follow host protein degradation and the subsequent impact on the host-virus equilibrium continues to be a complex endeavor. Here we reveal the multifaceted role of the DNA damage response protein RAP80 throughout HSV-1’s infection cycle. In early stages, RAP80 inhibits HSV-1 transcription by directly binding to the viral genome, blocking ICP4 (viral protein) binding to transcription factors. This interaction is regulated by phase separation via an intricate interplay between RAP80 and ICP0/ICP4. As infection progresses, the viral E3 ligase ICP0 degrades RAP80, dissolving phase separation, and allowing the formation of a mature viral replication compartment. In late infection stages, RAP80 is deubiquitinated by the viral deubiquitinase UL36USP, which restores cellular homeostasis and promotes HSV-1 survival. This process involves modulating the R-loop-cGAS-apoptosis pathway. These findings underscore the dynamic interplay between viral and host factors and the complex mechanisms used by HSV-1 to subvert host defenses, offering practical implications for the future development of antiviral strategies.

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RNA-seq identification of herpes simplex virus type 1 transcription in Neuro-2a cells overexpressing ONECUT2

Project description:This is a part of the study that shows that a host gene,ONECUT2 (OC2), promote herpes simplex virus 1 (HSV-1) transcription. These RNA-seq analyses viral genes transcription in Neuro-2a cells. Neuro-2a cells were transfected with pOC2△HOX2 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 5 hours.

2023-09-18 | GSE241029 | GEO

Effects of host miR-138 on herpes simplex virus 1 gene expression in Neuro-2a cells and their dependence of the binding sites on ICP0 mRNA

Project description:Effects of host miR-138 on herpes simplex virus 1 gene expression in Neuro-2a cells and their dependence of the binding sites on ICP0 mRNA

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Identification of SLFN5 as an intrinsic inhibitor of viral transcription antagonized by the herpes simplex virus ubiquitin ligase ICP0

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2020-09-14 | PXD018773 | Pride

Effects of the onecut family on herpes simplex virus 1 and host chromatin accessibility in Neuro-2a cells

Project description:This is a part of the study that shows that a host gene,ONECUT2( OC2), promotes herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses are for viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pOC2△HOX2 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 2 hours.

2023-09-18 | GSE240221 | GEO

Systems biology decodes herpes simplex virus 1

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2020-05-22 | PXD013407 | Pride

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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