Project description:The purpose of this study was to determine which genes are differentially regulated virus infection in RAW264.7 cells. Cells were infected with Vesicular Stomatitis Virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed, focusing on F-box proteins and E3 ubiquitin ligases. 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: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:The neurogenic niches within the central nervous system serve as essential reservoirs for neural precursor cells (NPCs), playing a crucial role in neurogenesis. However, these NPCs are particularly vulnerable to infection by the herpes simplex virus type 1 (HSV-1). In the present study, we investigated the changes in the transcriptome of NPCs in response to Herpes simplex virus 1 (HSV-1) infection. Using bulk RNA-Seq, the transcriptomes of HSV-1-infected NPCs were compared to those of uninfected samples at different time points in the presence or absence of antivirals.
Project description:We found that the germline transcription factor double homeobox 4 (DUX4) is upregulated upon infection with wild-type herpes simplex virus-1 (HSV-1). The goal of this experiment was to compare the cellular transcriptome of HEK293T cells that were infected with HSV-1 (KOS strain), or transfected with a plasmid encoding human DUX4.
Project description:The purpose of this study was to determine which genes are differentially regulated virus infection in RAW264.7 cells. Cells were infected with Vesicular Stomatitis Virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed, focusing on F-box proteins and E3 ubiquitin ligases.
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.
Project description:The purpose of this study was to determine what are the effects of TAO3 deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Tao3−/− 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.
Project description:Dendritic cells (DCs) regulate both innate and adaptive immune responses. The role of CD11c-plus DCs in the corneal response to to herpes simplex virus-1 (HSV-1) infection was investigated by depleting them prior to infection.
Project description:The goal of this study was to determine how RNA poymerase II (Pol II) occupancy changed in response to herpes simplex virus-1 (HSV-1) infection using ChIP-seq of Pol II. ChIP assays were performed 4 hours after cells were infected (or mock infected) with HSV-1. Because host cell Pol II transcribes the HSV-1 genome, the ChIP-seq data also reveal polymerase occupancy on the viral genome.
Project description:Dendritic cells (DCs) regulate both innate and adaptive immune responses. The role of CD11c-plus DCs in the corneal response to to herpes simplex virus-1 (HSV-1) infection was investigated by depleting them prior to infection. Bone marrow cells from CD11c-DTR (C.FVB-Tg(Itgax-DTR/EGFP)57Lan/J) mice were transferred intravenously to irradiated BALB/cJ host mice. After 6 weeks, the bone marrow chimeric host mice were injected with diphtheria toxin (DT) to deplete CD11c-positive cells. Two days after injection, the mice were subjected to a standard corneal infection protocol using HSV-1.