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SARS-CoV-2 spike protein interacts with and activates TLR4

ABSTRACT: SARS-CoV-2 spike protein interacts with and activates TLR4

PROVIDER: PRJNA704706 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13780407_1.fastq.gz	Fastqsanger.gz
	SRR13780407_2.fastq.gz	Fastqsanger.gz
	SRR13780408_1.fastq.gz	Fastqsanger.gz
	SRR13780408_2.fastq.gz	Fastqsanger.gz
	SRR13780409_1.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 spike protein interacts with and activates TLR4

Project description:We here identified that the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils. Moreover, specific TLR4 or NFKB inhibitor, or knockout of MyD88 could significantly block IL-1B induction by spike protein. We thus reveal that spike protein of SARS-CoV-2 functions as a potent stimulus causing TLR4 activation and sepsis related abnormal responses.

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The SARS-CoV-2 Spike protein modifies the transcriptional profile of human cardiac pericytes

Project description:Human cardiac pericytes express the receptors for SARS-CoV-2 and contribute to microvascular dysfunction in COVID-19 patients. The SARS-CoV-2 capsid Spike protein seems to play a direct role in COVID-19 microangiopathy, but it is not known yet whether the Spike protein alone, without the infectious virus, can induce transcriptional alterations in pericytes. This study investigated the signalling pathways activated by the Spike protein in cultured human cardiac pericytes. We found that 309 RNA transcripts were significantly modulated in pericytes exposed to the Spike protein, with the upregulation of pathways linked to inflammation and viral infection.

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Project description:mRNA vaccination of individuals with prior SARS-CoV-2 infection provides superior protection against breakthrough infections with variants of concern compared to vaccination in the absence of prior infection. However, the immune mechanisms by which this ‘hybrid immunity’ is generated and maintained are unknown. While genetic variation in spike glycoprotein effectively subverts neutralizing antibodies, spike-specific T cells are generally maintained against SARS-CoV-2 variants. Thus, we comprehensively profiled T cell responses against the S1 and S2 domains of spike glycoprotein in a cohort of SARS-CoV-2-naive or convalescent individuals who received two-dose mRNA vaccine series and were matched by age, sex, and vaccine type. Using flow cytometry, we observed that the overall functional breadth of CD4 T cells as well as polyfunctional Th1 responses were similar between the two groups. However, polyfunctional cytotoxic CD4 T cell responses against both S1 and S2 domains trended higher among convalescent subjects. Multi-modal single-cell RNA sequencing revealed diverse functional programs in spike-specific CD4 and CD8 T cells in both groups. However, convalescent individuals displayed enhanced cytotoxic and antiviral CD8 T cell responses to both S1 and S2 in the absence of cytokine production. Taken together, our data suggest that cytotoxic CD4 and CD8 T cells targeting spike glycoprotein may partially account for hybrid immunity and protection against breakthrough infections with SARS-CoV-2.

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