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Bulk RNA-seq of MHV-A59 infection in primary murine macrophages

ABSTRACT: Bulk RNA-seq of MHV-A59 infection in primary murine macrophages

PROVIDER: PRJNA770889 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16312645_1.fastq.gz	Fastqsanger.gz
	SRR16312645_2.fastq.gz	Fastqsanger.gz
	SRR16312646_1.fastq.gz	Fastqsanger.gz
	SRR16312646_2.fastq.gz	Fastqsanger.gz
	SRR16312647_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of MHV-A59 infection in primary murine macrophages

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dsRNA IP of Coronavirus Infected IFNAR-/- BMDMs

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RiboSeq of murine 17Cl-1 cells infected at MOI 10 with MHV-A59, compared to mock-infected controls, harvested at 5 and 8 hpi, plus a control tunicamycin-treated sample.

Project description:Murine 17Cl-1 cells were infected with the model Betacoronavirus mouse hepatitis virus (MHV) strain A59 and subjected to ribosome profiling to observe changes in the host translatome in infected cells compared to mock-infected cells. Samples were harvested at 5 and 8 hpi by flash-freezing, without cycloheximide pre-treatment. RNase I treatment was carried out, following which ribosomes and enclosed RNA were isolated by centrifugation through a sucrose cushion. RNA was extracted, ribosomal RNA was removed using Illumina's RiboZero kit, and remaining RNA was gel purified to select fragments 25-35nt long. Fragments were cloned into adapters using the TruSeq small RNA adapter kit and sequenced on Illumina NextSeq, then differential translation efficiency analysis was carried out on the data deposited data. One uninfected sample was treated with 2ug/mL tunicamycin for 6 hours before harvesting as a positive control for unfolded protein response activation.

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Transcription profiling of mouse fibroblasts infected with murine hepatitis virus using two array platforms to compare the potential for interference from viral RNA

Project description:Infection of cells with murine hepatitis virus strain A59 (MHV-A59) results in massive amounts of viral RNA within infected cells. When applying transcriptional profiling by means of microarray analysis, this could potentially cause problems since high amounts of viral RNA could in theory interfere with the analysis. Since coronavirus RNAs are polyadenylated, the viral RNAs are also amplified by oligo(dT) primers (a standard procedure when processing RNA samples for array hybridization). In this experiment we compared two different array platforms for the potential interference of viral RNA, using MHV-A59 infection of LR7 (murine fibroblasts) as a model.

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Gene Expression Timecourse of WT, DUBmut, and EndoUmut Mouse Hepatitis Virus Strain A59 infected C57bl/6 Bone Marrow derived macrophages

Project description:We report the differences in innate immune activation in the comparison of wild type and mutant Mouse Hepatitis Virus Strain A59 infection of bone marrow derived macrophages. We infected BMDMs and harvested RNA at 3, 6, 9, and 12 hpi while comparing changes in host gene expression compared to mock infected cells. Here, using a transcriptomics approach, we compared the scope and kinetics of the host response to the wild type, DUBmut, and EndoUmut viruses in infected macrophages. We found that the EndoUmut virus activates a focused response, predominantly involving type I interferons and a subset of interferon-responsive genes, within 12 hours after infection. In contrast, the wild type and DUBmut viruses stimulate the upregulation of over 2,800 genes, including the activation of unfolded protein response (UPR) pathways and a proinflammatory response associated with viral pathogenesis. This study highlights the role of viral interferon antagonists in modulating the kinetics and magnitude of the host response during virus infection and demonstrates that inactivation of a dominant viral antagonist, the coronavirus endoribonuclease, dramatically alters the host response in macrophages and the disease process.

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Pseudoxanthomonas spadix BD-a59

Project description:Pseudoxanthomonas spadix BD-a59 Genome sequencing project

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RNASeq of murine 17Cl-1 cells infected at MOI 10 with MHV-A59, compared to mock-infected controls, harvested at 5 and 8 hpi.

Project description:RNASeq of murine 17Cl-1 cells infected at MOI 10 with MHV-A59, compared to mock-infected controls, harvested at 5 and 8 hpi.

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Amino acid substitutions and an insertion in the spike glycoprotein extend the host range of the murine coronavirus MHV-A59.

Project description:The murine coronavirus [murine hepatitis virus (MHV)] is limited to infection of susceptible mice and murine cell lines by the specificity of the spike glycoprotein (S) for its receptor, murine carcinoembryonic antigen cell adhesion molecule 1a (mCEACAM1a). We have recently shown that 21 aa substitutions and a 7-aa insert in the N-terminal region of S are associated with the extended host range of a virus variant derived from murine cells persistently infected with the A59 strain of MHV (MHV-A59). We used targeted RNA recombination (TRR) to generate isogenic viruses that differ from MHV-A59 by the 21 aa substitutions or the 7-aa insert in S. Only viruses with both the 21 aa substitutions and the 7-aa insert in S infected hamster, feline, and monkey cells. These viruses also infected murine cells in the presence of blocking anti-mCEACAM1a antibodies. Thus, relatively few changes in the N-terminal region of S1 are sufficient to permit MHV-A59 to interact with alternative receptors on murine and non-murine cells.

| S-EPMC7127820 | biostudies-literature

PLP2 of mouse hepatitis virus A59 (MHV-A59) targets TBK1 to negatively regulate cellular type I interferon signaling pathway.

Project description:BACKGROUND:Coronaviruses such as severe acute respiratory syndrome (SARS) coronavirus (SCoV) and mouse hepatitis virus A59 (MHV-A59) have evolved strategies to disable the innate immune system for productive replication and spread of infection. We have previously shown that papain-like protease domain 2 (PLP2), a catalytic domain of the nonstructural protein 3 (nsp3) of MHV-A59, encodes a deubiquitinase (DUB) and inactivates IFN regulatory factor 3 (IRF3) thereby the type I interferon (IFN) response. PRINCIPAL FINDINGS:Here we provide further evidence that PLP2 may also target TANK-binding kinase-1 (TBK1), the upstream kinase of IRF3 in the IFN signaling pathway. Overexpression experiments showed that PLP2 deubiquitinated TBK1 and reduced its kinase activity, hence inhibited IFN-? reporter activity. Albeit promiscuous in deubiquitinating cellular proteins, PLP2 inactivated TBK1 and IFN-? response in TNF receptor associated factor 3 (TRAF3) deficient cells, suggesting that targeting TBK1 would be sufficient for PLP2 to inhibit IRF3 activation. This notion was further supported by in vitro kinase assays, in which prior treatment of TBK1 with PLP2 inhibited its kinase activity to phosphorylate IRF3. Intriguing enough, results of PLP2 overexpression system and MHV-A59 infection system proved that PLP2 formed an inactive complex with TBK1 and IRF3 in the cytoplasm and the presence of PLP2 stabilized the hypo-phosphorylated IRF3-TBK1 complex in a dose-dependent manner. CONCLUSIONS:These results suggest that PLP2 not only inactivates TBK1, but also prevents IRF3 nuclear translocation hence inhibits IFN transcription activation. Identification of the conserved DUB activity of PLP2 in suppression of IFN signaling would provide a useful clue to the development of therapeutics against coronaviruses infection.

| S-EPMC3041802 | biostudies-literature

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