Project description:Vesicular stomatitis virus replicates with marked effciency in Ifit2 knockout mouse brains late after infection (6 days after intranasal inoculation), compared to wt brains. Changes in gene expression, especially of interferon-stimulated genes, between late in infection (at 6 d p.i.) compared to early during infection (2 d p.i.) were examined in comparison to wild-type. Total RNA extracted from mouse brains of wt or Ifit2 knockout mice at 6 days after infection, compared to RNA from 2 days after infection.
Project description:Vesicular stomatitis virus replicates with marked effciency in Ifit2 knockout mouse brains late after infection (6 days after intranasal inoculation), compared to wt brains. Changes in gene expression, especially of interferon-stimulated genes, between late in infection (at 6 d p.i.) compared to early during infection (2 d p.i.) were examined in comparison to wild-type.
Project description:Sarm-deficient mice are protected from VSV encephalitis and death. Microarray was done to examine genes contributing to this phenotype WT and KO mice were infected with VSV and brains were harvested at day 5 post-infection for RNA extraction
Project description:To investigate the function of XAF1 in chromatin openning. Wild-type or XAF1 knockout HT29 cells were infected with VSV for 0 or 3 hours,ATAC-seq was performed. Examination of chromatin openness in Wild-type or XAF1 knockout HT29 cells.
Project description:To investigate whether and what miRNAs expression might be regulated by VSV (vesicular stomatitis virus?) challenge, we analyzed the miRNA expression profile of mouse primary peritoneal macrophages infected with VSV by using an array-based miRNA profiling. After the infection of VSV at MOI 10 for 48 h, the array revealed that many miRNAs were up-regulated in macrophages?
Project description:The goal of this study is to compare transcriptome-wide Nm-seq on the poly A+ RNA of wild-type Raw264.7 macrophages to transcriptome-wide Nm-seq on the poly A+ RNA of Raw264.7 macrophages after VSV infection . The Nm-seq profiles of wild-type Raw264.7 poly A+ RNA and VSV infected Raw264.7 poly A+ RNA were generated by deep sequencing using Illumina HiSeq4000 sequencer.
Project description:Cells infected by influenza virus mount a large-scale antiviral response and most cells ultimately initiate cell-death pathways in an attempt to suppress viral replication. We performed a CRISPR/Cas9-knockout selection designed to identify host factors required for replication following viral entry. We identified a large class of presumptive antiviral factors that unexpectedly act as important pro-viral enhancers during influenza virus infection. One of these, IFIT2, is an interferon-stimulated gene with well-established antiviral activity but limited mechanistic understanding. As opposed to suppressing infection, we show here that IFIT2 is instead repurposed by influenza virus to promote viral gene expression. CLIP‐seq demonstrated that IFIT2 binds directly to viral and cellular mRNAs in AU‐rich regions, with bound cellular transcripts enriched in interferon‐stimulated mRNAs. Polysome and ribosome profiling revealed that IFIT2 prevents ribosome pausing on bound mRNAs. Together, the data link IFIT2 binding to enhanced translational efficiency for viral and cellular mRNAs and ultimately viral replication. Our findings establish a model for the normal function of IFIT2 as a protein that increases translation of cellular mRNAs to support antiviral responses and explain how influenza virus uses this same activity to redirect a classically antiviral protein into a pro-viral effector.
Project description:Human SLK cells were infected with wildtype (wt) and LANA knockout (KO) Kaposi's sarcoma-associated herpesvirus (KSHV), separately for 3 days. Cellular gene expression changes were identified upon the wild type and LANA KO KSHV virus infection compared to the uninfected SLK cells using the human gene expression microarray U133plus2.0.
Project description:Wild type or HIPK2-/- immortalized bone marrow-derived macrophages (iBMDM) were infected with VSV for 6h, followed by whole genome RNA-seq analysis. Conclusions: HIPK2 deficiency aggravates viral infection and inhibited the production of IFNβ.
Project description:Human SLK cells were infected with wildtype (wt) and LANA knockout (KO) Kaposi's sarcoma-associated herpesvirus (KSHV), separately for 3 days. Cellular gene expression changes were identified upon the wild type and LANA KO KSHV virus infection compared to the uninfected SLK cells using the human gene expression microarray U133plus2.0. 2 independent biological replicates from uninfected SLK cells, wild type KSHV infected SLK cells at 72hrs post-infection (hpi) , and LANA KO infected SLK cells at 72 hrs post-infection were collected and RNA was prepared for microarray analysis.
