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ABSTRACT: SFTSV-infected THP-1

PROVIDER: PRJNA1086175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28284612_1.fastq.gz	Fastqsanger.gz
	SRR28284612_2.fastq.gz	Fastqsanger.gz
	SRR28284613_1.fastq.gz	Fastqsanger.gz
	SRR28284613_2.fastq.gz	Fastqsanger.gz
	SRR28284614_1.fastq.gz	Fastqsanger.gz

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SFTSV exploits PPM1K to inhibit apoptosis through the Bcl-2/BAX/Caspase-3 axis for efficient replication

Project description:In this study, transcriptomic profiling identified PPM1K as a prominently induced host factor in SFTSV-infected THP-1 cells. We further demonstrate that SFTSV infection promotes endoplasmic reticulum–mitochondria coupling, enabling the viral glycoprotein GC to interact with mitochondrial PPM1K and enhance its expression at both transcriptional and protein levels. Mechanistically, PPM1K dephosphorylates Bcl-2 at Ser248, decreases Bcl-2 ubiquitination, and stabilizes its anti-apoptotic activity, thereby suppressing the BAX–Caspase-3 signaling cascade. This anti-apoptotic remodeling markedly limits apoptosis in infected cells and facilitates efficient SFTSV replication. These findings uncover a previously unrecognized viral strategy in which SFTSV hijacks host PPM1K-dependent mitochondrial signaling to evade apoptosis and promote replication

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Project description:Severe fever with thrombocytopenia syndrome (SFTS) is a new tick-borne infectious disease caused by a new SFTS virus (SFTSV). Due to its 12%-50% high fatality rate and the possibility of pandemic transmission, as well as no specific antiviral drugs for the treatment so far, SFTSV has been listed as one of the top 10 priority infectious diseases by the World Health Organization. Currently, there are rare studies of transcriptomic analysis for the patients infected with SFTSV, which makes it difficult to deeply understand the life cyle and pathogenicity of this virus. To explore the differences of transcripts after SFTSV infection, we performed a longitudinal sampling study to systematically investigate the chronological changes of viral load and transcriptomic and epigenetic characterization using white blood cells from SFTSV patients. The results showed significant changes in the expression of some genes from onset to recovery of SFTSV infection. Moreover, these differentially expressed genes showed good consistency in the three patients at different stages of treatment, which may contribute to the pathophysiology of SFTSV and thus lead to a breakthrough in SFTSV therapy. Moreover, by m6A-seq, we found some genes that might be regulated by m6A. This study in transcript changes and RNA modification may open a brand new direction to our understanding of SFTSV and play an important role in the drugs discovery for effective treatment.

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