Project description:To discover the mechanism by which herpes simplex virus type 1 (HSV-1) drastically reshapes the host cell transcriptional patterns during infection, we performed RNAseq. We infected A549 cells with HSV-1, and analized host and viral expression at 1, 3 and 8 hours post infection. We report both a drastical human transcription shutoff parallel with an increase in viral transcription.
Project description:The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.
Project description:This is a part of the study that shows that a host gene,FOXF1, promote herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pFOXF1 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 3 hours.
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.
Project description:We show that Herpes simplex virus 1 (HSV-1) induces the expression of about 1000 antisense transcripts from the human host cell genome.
Project description:Infection by viruses, including Herpes Simplex virus-1 (HSV-1), and cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII). The underlying mechanisms, however, remain unclear. Here we demonstrate that, in HSV-1-infected cells, the viral immediate early factor ICP27 is necessary and sufficient for inducing DoTT. Mechanistically, ICP27 directly binds to the essential mRNA 3’ processing factor CPSF, induces the assembly of a dead-end 3’ processing complex, and blocks mRNA cleavage. Remarkably, ICP27 also acts as a sequence-dependent activator of mRNA 3’ processing for HSV-1 and a subset of host genes. Our results suggest that the bimodal activities of ICP27 play a key role in HSV-1-induced host shutoff and that CPSF is a common host factor targeted by multiple viruses. The mechanism described here may have implications for understanding other virus- and cell stress-mediated regulation of transcription termination.
2019-12-15 | GSE128753 | GEO
Project description:Antiviral resistance evolution in hypermutator herpes simplex virus
