Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1123273 | ENA |
REPOSITORIES: ENA
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Project description:Genome wide RNA-Seq screen was did to detect gene expression. We used immortalized bone-marrow-derived macrophages cells that were uninfected or infected with HSV-1 for 6 hours to detect the expression levels of genes, and we found that interferon stimulated genes were increased and some of genes that inhibit interferon production were decreased in HSV-1 infected iBMDMs, compared to wild-type iBMDMs. we choose some genes that are unknown about their functions on antiviral innate immunity, and adress how they participate in antiviral innate immunity.
2018-10-11 | GSE121061 | GEO
Project description:Administration of recombinant interferons to 3D brain organoid cultures infected with HSV reveals a strong antiviral effect of IFN-alpha against HSV
2021-04-09 | GSE145496 | GEO
Project description:Recently, we reported that expression of endogenous retroviruses (ERVs), a class of transposable element, is associated with response to immune checkpoint blockade (ICB) in renal cell carcinoma (RCC). Aberrant expression of ERVs can activate host antiviral responses, as well as produce neoantigens. ERV expression is repressed by DNA methylation and can be activated by DNA hypomethylating agents. Here, we investigate whether Decitabine, a DNA hypomethylating agent, can activate ERV expression and host antiviral defenses in RCC to potentially enhance response to ICB. Decitabine induced expression of ERV3-2 and ERV4700 in RCC cells lines, which was accompanied by activation of host antiviral defense genes and increased secretion of inflammatory cytokines. We validated this effect in primary human RCC cell lines. Knockout of RIG-I and MDA5 dsRNA sensors attenuated activation of antiviral responses associated with Decitabine treatment, and RIG-I and MDA5 immunoprecipitations showed increased ERV binding in RCC cells treated with Decitabine. Bioinformatic analysis of RNAseq data showed the Decitabine-induced gene signature could be associated with increased CD8 infiltration and response to ICB. Conditioned media from Decitabine treated RCC cells was capable of inducing host anti-viral defense in naïve RCC cells and could modestly improve activation of T-cells from healthy donors. Further, conditioned media from RCC cells treated with Decitabine significantly enhanced T-cell migration. In a small retrospective cohort of metastatic RCC patients treated with single-agent PD-1/PD-L1 blockade, activation of some host antiviral defense genes was significantly higher in responders compared with nonresponders. Thus, modulation of ERV expression by Decitabine to activate host antiviral defenses could represent a novel therapeutic strategy to enhance RCC patient response to immune checkpoint blockade.
2020-06-01 | GSE142381 | GEO
Project description:Evolution of drug-resistant hepatitis C virus clones during direct-acting antiviral therapy.
| PRJDB5184 | ENA
Project description:Purpose: The global effort to combat COVID-19 rapidly produced a shortlist of approved drugs with anti-viral activities for clinical repurposing. However, the jump to clinical testing was lethal in some cases since a full understanding of the mechanism of antiviral activity as opposed to inherent toxicity for these drugs was lacking. We used parallel lipidomic and transcriptomic analyses to investigate the effect of Niclosamide (NIC), a poorly soluble anti-helminth drug identified for repurposed treatment of COVID-19, on SARS-CoV-2 infected Vero E6 cells. Methods: A time of addition study was performed on VeroE6 cells to gain mRNA profiles of 16 and 48h SARS-CoV-2 and/or niclosamide infected cells in triplicate, using an Illumina NovaSeq6000 platfrom. Sequence reads that passed quality filters were analyzed by featurecounts and DESeq2. Results: Herein, we identified and characterized autophagic or lipophagic pathways (and wider linked cellular networks) that are targeted by NIC in the presence and absence of a SARS-CoV-2 infection. We used the lipid and gene expression signatures induced by this anti-parasitic compound to detect pathways that are predicted to either lead to direct antiviral effects or to cellular dysregulation and cell death. Conclusions: NIC treatment reduced the abundance of phosphatidylethanolamines (PE), a known activator of autophagy, only after establishment of SARS-CoV-2 infection. Countering SARS-CoV-2 subversion of lipid metabolism by NIC through the activation of PE may lead to a focused screen for approved, more druggable compounds that can suppress viral replication in COVID-19 patients.
2023-10-01 | GSE178157 | GEO
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.
2016-07-01 | E-GEOD-81675 | biostudies-arrayexpress
Project description:Type III interferons (IFN-λ) are antiviral and immunomodulatory cytokines that have been best characterized in respiratory and gastrointestinal infections, but the effects of IFN-λ against skin infections have not been extensively investigated. We sought to define the skin-specific effects of IFN-λ against the highly prevalent human pathogen herpes simplex virus (HSV). We infected mice lacking the IFN-λ receptor (Ifnlr1-/-), both the IFN-λ and the IFN-αβ receptor (Ifnar1-/- Ifnlr1-/-), or IFN-λ cytokines (Ifnl2/3-/-) and found that IFN-λ restricts the severity of HSV-1 and HSV-2 skin lesions, independent of a direct effect on viral load. Using conditional knockout mice, we found that IFN-λ signaling in both keratinocytes and neutrophils was necessary to control HSV-1 skin lesion severity, and that IFN-λ signaling in keratinocytes suppressed CXCL9-mediated neutrophil recruitment to the skin. Furthermore, depleting neutrophils prevented the development of severe HSV-1 skin lesions in Ifnlr1-/- mice. Altogether, our results suggest that IFN-λ plays an immunomodulatory role in the skin that restricts neutrophil-mediated pathology during HSV infection, and suggest potential applications for IFN-λ in treating viral skin infections.
2023-09-12 | GSE242170 | GEO
Project description:Type III interferons (IFN-λ) are antiviral and immunomodulatory cytokines that have been best characterized in respiratory and gastrointestinal infections, but the effects of IFN-λ against skin infections have not been extensively investigated. We sought to define the skin-specific effects of IFN-λ against the highly prevalent human pathogen herpes simplex virus (HSV). We infected mice lacking the IFN-λ receptor (Ifnlr1-/-), both the IFN-λ and the IFN-αβ receptor (Ifnar1-/- Ifnlr1-/-), or IFN-λ cytokines (Ifnl2/3-/-) and found that IFN-λ restricts the severity of HSV-1 and HSV-2 skin lesions, independent of a direct effect on viral load. Using conditional knockout mice, we found that IFN-λ signaling in both keratinocytes and neutrophils was necessary to control HSV-1 skin lesion severity, and that IFN-λ signaling in keratinocytes suppressed CXCL9-mediated neutrophil recruitment to the skin. Furthermore, depleting neutrophils prevented the development of severe HSV-1 skin lesions in Ifnlr1-/- mice. Altogether, our results suggest that IFN-λ plays an immunomodulatory role in the skin that restricts neutrophil-mediated pathology during HSV infection, and suggest potential applications for IFN-λ in treating viral skin infections.
2023-09-12 | GSE242068 | GEO
Project description:RNAseq experiments of Enterovirus A71 wild type demonstrate that the pyrazine-carboxamide ribonucleotide stimulates catalyzed intra- and intermolecular template switching. These results suggest that pyrazine-2 carboxamide ribonucleotides do not induce lethal mutagenesis or chain termination, but function by promoting template switching and formation of defective viral genomes. We conclude that RdRp-catalyzed intra- and intermolecular template switching can be induced by pyrazine-carboxamide ribonucleotides, defining an additional mechanistic class of antiviral ribonucleotides with potential for broad-spectrum activity.
2021-09-14 | GSE183959 | GEO