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Analysis of SFTS pathogenesis based on single-cell RNA sequencing of monocytes

ABSTRACT: Analysis of SFTS pathogenesis based on single-cell RNA sequencing of monocytes

PROVIDER: PRJNA1214776 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32095305_1.fastq.gz	Fastqsanger.gz
	SRR32095305_2.fastq.gz	Fastqsanger.gz
	SRR32095306_1.fastq.gz	Fastqsanger.gz
	SRR32095306_2.fastq.gz	Fastqsanger.gz
	SRR32095307_1.fastq.gz	Fastqsanger.gz

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Analysis of SFTS pathogenesis based on single-cell RNA sequencing of monocytes

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Project description:We performed scRNA-seq on 27 PBMC samples from 15 SFTS patients (including four deceased and 11 surviving) and four healthy controls. We found that the immune cell landscape was reprogrammed in SFTS and characterized by monocyte shift to intermediate type along with complement activation, perturbation of plasmablasts composition, and highly exhausted T cells, all were correlated with lethal consequences. We identified the overexpression of interferon-stimulated genes across most immune cell types post SFTSV infection, which were simultaneously related to older age, high viremia and hyper-inflammation. These data collectively supported the intermediate monocytes and IFN-I-inducible plasmablasts to be major targets for SFTSV infection, and proposed the pivotal role of IFN-I response in exacerbating hyper-inflammation and lethal SFTS, which might help to identify therapeutic strategies for SFTS.

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Transcriptomic analysis of blood samples collected from SFTS patients

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Project description:Severe fever with thrombocytopenia syndrome banyangvirus (SFTSV) induces immunopathogenic disease with high fatality rate. Despite serious health concern, the mechanisms underlying clinical manifestations are largely unknown. Here, we applied targeted proteomics and single-cell transcriptomics analyses to examine the differential immune landscape of SFTS patient blood. Serum immunoprofiling distinguished Low-risk and High-risk clusters of SFTS patients with differential inflammatory cytokine levels, which matched with disease severity. Single-cell transcriptomics analysis of SFTS patient blood at different infection state showed pronounced expansion of B cells with the alteration of B-cell subset populations, specifically in fatal patients. Furthermore, plasma cells were the primary reservoir of SFTSV replication with the downregulation of IFN pathway. This study identifies not only the molecular signatures of serum inflammatory profile and B cell lineage population, but also plasma cells as the viral reservoir in SFTSV-induced fatal patients, suggesting the alteration of B cell function linked to SFTS lethal infection.

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