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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

ABSTRACT: We use the a porcine genome-scale CRISPR/Cas9 knockout (PigGeCKO) library (Zhao et al., 2020) to identify key host factors facilitating TGEV infection in porcine cells.

ORGANISM(S): Sus scrofa

PROVIDER: GSE169111 | GEO | 2021/11/19

REPOSITORIES: GEO

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

Project description:We use the Focused-library to identify key host factors facilitating TGEV infection in porcine cells.

2021-11-19 | GSE169108 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

Project description:Explore the potential downstream signaling pathways that inhibit TGEV replication after knocking out TMEM41B by RNA-seq analysis.

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-19 | GSE169113 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a multi-function host factor required for coronavirus replication.

Project description:Emerging coronaviruses (CoVs) pose a severe threat to human and animal health worldwide. To identify host factors required for CoV infection, we used α-CoV transmissible gastroenteritis virus (TGEV) as a model for genome-scale CRISPR knockout (KO) screening. Transmembrane protein 41B (TMEM41B) was found to be a bona fide host factor involved in infection by CoV and three additional virus families. We found that TMEM41B is critical for the internalization and early-stage replication of TGEV. Notably, our results also showed that cells lacking TMEM41B are unable to form the double-membrane vesicles necessary for TGEV replication, indicating that TMEM41B contributes to the formation of CoV replication organelles. Lastly, our data from a mouse infection model showed that the KO of this factor can strongly inhibit viral infection and delay the progression of a CoV disease. Our study revealed that targeting TMEM41B is a highly promising approach for the development of broad-spectrum anti-viral therapeutics.

| S-EPMC8675922 | biostudies-literature

Long-term Expansion of Porcine Intestinal Organoids serves as an Ex Vivo Model for Swine Enteric Coronavirus infection

Project description:We designed a long-term culture system for porcine intestinal organoids from intestinal crypt or single Lgr5+ stem cells by combining previously defined insights in the growth requirements of intestinal epithelium of human and mouse. We showed that long-term cultured swine intestinal organoids were expanded in vitro more than six months at least and maintained the potential to differentiate into different types of cells. These organoids were successfully infected with porcine enteric coronavirus including porcine epidemic diarrhea virus (PEDV) and transmissible gastroenteritis virus (TGEV). RNA-seq analysis showed that robust induction of transcripts associated with antiviral signaling in response to enteric coronavrius infection, including a number of interferon-stimulated genes and cytokines. Moreover, gene set enrichment analysis indicated that PEDV infection could suppress immune response in organoids. This 3D intestinal organoid model offers a long-term, renewable resource for investigating porcine intestinal infections with a variety of pathogens.

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Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

| PRJNA715232 | ENA

Receptor Tyrosine Kinase Inhibitors Block proliferation of coronavirus mainly through p38 mitogen-activated protein kinase pathways

Project description:Emerging coronaviruses (CoVs) primarily cause severe gastroenteric or respiratory diseases in humans and animals, for which no approved therapeutics are available so far. Here A9, a receptor tyrosine kinase inhibitors (RTKIs) of the tyrphostin class was identified as a robust inhibitor of TGEV (Transmissible gastroenteritis virus) infection in cell-based assays. Time-of-addition studies suggested that A9 mainly acts at post-adsorption stage of the TGEV life cycle. Moreover, it also exhibited potent antiviral activity against various coronavirus replication, including MHV, PEDV and FIPV. We further investigated the mechanism of action of A9 against TGEV infection in vitro with comparative phosphoproteomics analysis. We specifically identified the A9 target, p38 and JNK1, the downstream molecules of receptor tyrosine kinases (RTKs) as required for efficient TGEV replication in vitro through plaque assay, qRT-PCR and western blotting assays. Additionally, tests of p38 and JNK1 inhibitors also indicated that interventions targeting p38 was more effective in suppressing TGEV propagation than the JNK. In conclusion, these findings indicate that the receptor tyrosine kinase inhibitor A9 can directly inhibits TGEV replication and its inhibitory activity on TGEV replication mainly regulated by targeting p38, which provide vital clues to design novel drugs against coronavirus.

2020-05-26 | PXD010685 | Pride

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

| PRJNA715228 | ENA

The porcine microRNA transcriptome response to transmissible gastroenteritis virus infection

Project description:Transmissible gastroenteritis virus (TGEV; Coronaviridae family) causes huge economic losses to the swine industry. MicroRNAs (miRNAs) play a regulatory role in viral infection and may be involved in the mammalian immune response. Here, we report a comprehensive analysis of host miRNA expression in TGEV-infected swine testis (ST) cells. Deep sequencing generated 3,704,353 and 2,763,665 reads from uninfected ST cells and infected ST cells, respectively. The reads were aligned to known Sus scrofa pre-miRNAs in miRBase 19, identifying 284 annotated miRNAs. Certain miRNAs were differentially regulated during TGEV infection, which confirmed the hypothesis that specific miRNAs play a regulatory role in virus-host interactions. 59 unique miRNAs displayed significant differentially expression between the normal and TGEV-infected ST cell samples: 15 miRNAs were significantly up-regulated and 44 were significantly down-regulated. Stem-loop RT-PCR was carried out to determine the expression levels of specific miRNAs in the two samples, and the results were consistent with those of sequencing. Gene ontology enrichment analysis of host target genes demonstrated that the differentially expressed miRNAs are involved in regulatory networks, including cellular process, metabolic process, immune system process. This is the first report of the identification of ST cell miRNAs and the comprehensive analysis of the miRNA regulatory mechanism during TGEV infection, which revealed the miRNA molecular regulatory mechanisms for the viral infection, expression of viral genes and the expression of immune-related genes. The results presented here will aid research on the prevention and treatment of viral diseases. 2 ST(Porcine testicular cells) cell samples, ST: normal ST cell sample (contro sample), TGEV: TGEV (Transmissible gastroenteritis virus) infected ST cell samples

2015-01-08 | E-GEOD-64737 | biostudies-arrayexpress

Expression data from porcine cells infected with TGEV wild-type (rTGEV-wt) or mutant (rTGEV-delta7) coronaviruses

Project description:Innate immune response is the first line of antiviral defense resulting, in most cases, in pathogen clearance with minimal clinical consequences. Viruses have developed diverse strategies to evade innate immune response and to ensure their survival. Using transmissible gastroenteritis virus (TGEV) as a model, we previously reported that accessory gene 7 counteracts host antiviral response by its association with the catalytic subunit of protein phosphatase 1 (PP1c). A transcriptomic analysis was performed to further investigate the effect of gene 7 absence on the host cell. A recombinant TGEV virus lacking gene 7 expression (rTGEV-delta7) was previously generated in our laboratory. Porcine ST cells were mock infected or infected with wild type (rTGEV-wt) or mutant (rTGEV-delta7) virus. Gene expression was analyzed at 6 and 12 hours post infection (hpi) by using porcine Affymetrix microarray. Three biological replicates were made for each sample type.

2013-09-30 | E-GEOD-41756 | biostudies-arrayexpress

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