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SARS-CoV-2 proteins inhibit mitochondrial HIGD1A to induce complement-mediated endothelial cell injury

ABSTRACT: SARS-CoV-2 proteins inhibit mitochondrial HIGD1A to induce complement-mediated endothelial cell injury

PROVIDER: PRJNA950064 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24007745_1.fastq.gz	Fastqsanger.gz
	SRR24007745_2.fastq.gz	Fastqsanger.gz
	SRR24007746_1.fastq.gz	Fastqsanger.gz
	SRR24007746_2.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 proteins inhibit mitochondrial HIGD1A to induce complement-mediated endothelial cell injury

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Project description:Cancer metastasis remains one of the major causes of cancer deaths. The molecular mechanisms of pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, our RNA seq data showed that S1PR1 overexpression B16 melanoma cells injected in C57BL/6 mice via tail vein, activates endogenous complement signaling and inflammasome to induce tumor lung metastasis.

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Project description:Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here we uncover a role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.

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SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.

Project description:Complement hyperactivation and thrombotic microangiopathy are closely associated with severe COVID-19. Endothelial dysfunction is a key mechanism underlying thrombotic microangiopathy. To address the relationship between endothelial injury, complement activation and thrombotic microangiopathy of severe COVID-19, we wonder whether, and if so, what and how SARS-CoV-2 factors make endothelial cells (ECs) sensitive to complement-mediated cytotoxicity. We revealed that multiple SARS-CoV-2 proteins enhanced complement-mediated cytotoxicity to ECs by inhibiting membrane complement regulatory proteins (CRPs) and enhancing the deposition of complement-recognizing component FCN1. By screening with CRISPR/Cas9-gRNA libraries, we identified that ADAMTS9, SYAP1, and HIGD1A as intrinsic regulators of CD59 on ECs, which were inhibited by the SARS-CoV-2 M, NSP16, and ORF9b proteins. IFN-γ, GM-CSF, and IFN-α upregulated CD55 and CD59, while IFN-γ antagonized the inhibition of CD59 by the three SARS-CoV-2 proteins. So, the deficiency of IFN-γ weakened the protection of ECs by CRPs against complement-mediated injury which may be enhanced during infection. Our findings illustrated the regulation of protection against complement-mediated attack on self-cells by SARS-CoV-2 infection and immune responses, providing insights into endothelial injury, thrombotic microangiopathy, and potential targets for treating severe COVID-19.

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