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Herpes Simplex Virus blocks host transcription termination via the bimodal activities of ICP27.

ABSTRACT: Herpes Simplex Virus blocks host transcription termination via the bimodal activities of ICP27.

PROVIDER: PRJNA528792 | ENA |

REPOSITORIES: ENA

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Herpes Simplex Virus blocks host transcription termination via the bimodal activities of ICP27.

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

Herpes simplex virus blocks host transcription termination via the bimodal activities of ICP27.

Project description: Not available

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Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation

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Herpes simplex host shutoff attenuates antiviral state

Project description:Herpes simplex virus mutants lacking the vhs gene are severely attenuated in animal models of pathogenesis and exhibit reduced growth in primary cell culture. As a result of these properties vhs-deleted virus have been proposed as live-attenuated viruses. Despite these findings and their implications for vacccines, the mechanisms by which vhs promotes infection in cell culture and in vivo are not understood. In this study we demonstrate that vhs-deficent viruses replicate to reduced levels in interferon(IFN)- primed cells. Furthermore, vhs-defective viruses induce increased levels of IFN? and IFN?-stimulated genes, and increased levels of eIF2? phosphorylation in infected cells. In addition, we demonstrate a generalized over-expression of viral RNAs following infection with a vhs-deficient virus. This suggests increased expression of IFN pathway inducing double stranded RNA, a potent pathogen-associated molecular pattern (PAMP). Together these data show that vhs likely functions to reduce innate immune responses and thereby acts as critical determinant of viral pathogenesis. Keywords: time course, genetic modification Time course (1,3,6,9 & 12h) of HSV infected mouse embryo fibroblasts. Wild type (KOS) virus is co-hybridized with vhs null virus (NHB). Each time-point is hybridized in quadruplicate.

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Glutamine supplementation suppresses herpes simplex virus reactivation

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RNA Helicase DDX3X Modulates Herpes Simplex Virus 1 Nuclear Egress

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