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Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

ABSTRACT: We have identified that the viral virulence factors ICP0 from HSV-1 and E4ORF3 from Adenovirus5 can activate the MORC3 pathway of innate immune sensing. To study the global transcriptional effects of virulence factor sensing, we overexpressed mCherry or these virulence factors from a doxycycline-inducible lentiviral construct in BLaER1 monocytes of various genotypes and performed RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182754 | GEO | 2021/11/01

REPOSITORIES: GEO

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Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

Project description:Transcriptional effects of HSV-1-ICP0 and Ad5-E4ORF3 expression in BLaER1 monocytes [Virulence factors]

| PRJNA757714 | ENA

Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]

Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global transcriptional effects of loss of MORC3, we deleted MORC3 in WT, IFNAR1–/– IFNAR2–/– and IFNB1–/– BLaER1 monocytes and performed RNA-seq.

2021-11-01 | GSE182755 | GEO

ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

Project description:We have identified MORC3 as a negative regulator of Type I Interferon (IFN), whose absence induces IFN and interferon-stimulated genes (ISGs). To study the global effects of MORC3 on DNA accessibility, we deleted MORC3 in IFNAR1-/- IFNAR2-/- BLaER1 monocytes and performed ATAC-seq.

2021-11-01 | GSE182752 | GEO

Transcriptional profile of MRE deficient BLaER1 monocytes [RNA MRE]

Project description:We have identified a MORC3-regulated DNA element (MRE) that regulates the activation of IFNB1 upon loss of MORC3. To study the global transcriptional effects of the MRE, we deleted the MRE in STAT1–/– STAT2–/– and STAT1–/– STAT2–/– MORC3–/– BLaER1 monocytes and performed RNA-seq.

2021-11-01 | GSE182753 | GEO

Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]

Project description:Transcriptional profile of MORC3 deficient BLaER1 monocytes [KO]

| PRJNA757713 | ENA

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

ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

Project description:ATAC-seq of MORC3 deficient BLaER1 monocytes [ATAC-seq]

| PRJNA757711 | ENA

TAP/MS of enriched ICP0 gel detection in human astroblastoma cells infected with HSV-1

Project description:TAP/MS of enriched ICP0 gel detection in human astroblastoma cells infected with HSV-1 to identify ICP0's interacting partners

2023-12-20 | PXD048021 | iProX

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

Project description:Intrinsic antiviral host factors are proteins that can confer cellular defense by limiting virus replication. Viruses hijack ubiquitin machinery to modify the cellular proteome to subvert these host defenses. The herpes simplex virus 1 (HSV-1) expresses ICP0, which functions as an E3 ubiquitin ligase required to promote infection. Cellular substrates of ICP0 have been discovered as host barriers to infection but the mechanisms for inhibition of viral gene expression are not fully understood. To identify new restriction factors antagonized by ICP0, we compared the proteomes associated with viral DNA (vDNA) during HSV-1 infection with wild-type (WT) virus and a mutant lacking functional ICP0 (ΔICP0). We identified the cellular protein Schlafen 5 (SLFN5) as a new ICP0 target that binds vDNA during HSV-1 ΔICP0 infection. We demonstrated that ICP0 mediates ubiquitination of SLFN5 which leads to its proteasomal degradation. In the absence of ICP0, we demonstrate SLFN5 binds vDNA to represses HSV-1 transcription by limiting accessibility of RNA polymerase II to viral promoters. These results identify SLFN5 as a new restriction factor that inhibits viral transcription and document the first viral countermeasure reported to overcome SLFN antiviral activity.

2020-09-14 | PXD018773 | Pride

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