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ABSTRACT: Genome-wide CRISPR Knockout Screen Identified PLAC8 as an Essential Factor for SADS-CoVs Infection

PROVIDER: PRJNA826466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18743636_1.fastq.gz	Fastqsanger.gz
	SRR18743636_2.fastq.gz	Fastqsanger.gz
	SRR18743637_1.fastq.gz	Fastqsanger.gz
	SRR18743637_2.fastq.gz	Fastqsanger.gz
	SRR18743638_1.fastq.gz	Fastqsanger.gz

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Genome-wide CRISPR Knockout Screen Identified PLAC8 as an Essential Factor for SADS-CoVs Infection

Project description:Genome-wide CRISPR Knockout Screen Identified PLAC8 as an Essential Factor for SADS-CoVs Infection

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Genome-wide CRISPR Knockout Screen Identified PLAC8 as an Essential Factor for SADS-CoVs Infection

Project description:Zoonotic transmission of coronaviruses poses an ongoing threat to human populations. Endemic outbreaks of Swine Acute Diarrhea Syndrome Coronavirus (SADS-CoV) have caused severe economic losses in the pig industry and have the potential to cause human outbreaks. Currently, there are no vaccines or specific antivirals against SADS-CoV, and our limited understanding of SADS-CoV host entry factors could hinder prompt responses to a potential human outbreak. Using a genome-wide CRISPR knockout screen, we identified placenta-associated 8 protein (PLAC8) as an essential host factor for SADS-CoV infection. Knockout of PLAC8 abolished SADS-CoV infection, which was restored by complementing PLAC8 from multiple species, including human, rhesus macaques, mouse, pig, pangolin, and bat, suggesting a conserved infection pathway and susceptibility of SADS-CoV among mammals. Mechanistically, PLAC8 knockout does not affect viral entry; rather, knockout cells displayed a delay and reduction in viral subgenomic RNA expression. In a swine primary intestinal epithelial culture (IEC) infection model, differentiated cultures have high levels of PLAC8 expression and support SADS-CoV replication. In contrast, expanding IEC have low levels of PLAC8 expression and are resistant to SADS-CoV infection. PLAC8 expression patterns translate in vivo; immunohistochemistry of swine ileal tissue revealed high levels of PLAC8 protein in neonatal compared to adult tissue, mirroring the known SADS-CoV pathogenesis in neonatal piglets. Overall, PLAC8 is an essential factor for SADS-CoV infection and may serve as a promising target for antiviral development for the potential pandemic SADS-CoV virus.

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Project description:SARS-CoV-2 pandemic has caused a dramatic health, social and economic crisis worldwide. To better understand the host-virus interactions and identify potentially targetable host factors, we have conducted CRISPR-Cas9 genetic screens using SARS-CoV-2 pseudotyped lentiviruses on human lung cancer cells. Our results recapitulate many findings from previous screens that used full SARS-CoV-2 viruses, but also unveil two novel critical host factors: SPNS1 and PLAC8. Functional experiments with full SARS-CoV-2 viruses have confirmed that loss-of-function of these genes impairs viral entry. Importantly, we have found that PLAC8 is a key limiting host factor whose overexpression boosts viral infection in eight different human lung cancer cell lines. Using single-cell RNA-Seq data analyses, we demonstrate that PLAC8 is highly expressed in ciliated and secretory cells from the respiratory tract and in gut enterocytes, cell types that are highly susceptible to SARS-CoV-2 infection. Finally, proteomics and cell biology studies suggest that SPNS1 and PLAC8 affect viral entry through regulation of autophagy and lysosomal function.

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