Dataset Information

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE328306 | GEO | 2026/04/21

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:RNA modification plays a crucial role in the regulation of various diseases and viral infections. ADAR1 (adenosine deaminase 1) is a key RNA editing enzyme that can convert adenosine (A) into the modified base inosine (I). This RNA modification has been confirmed to regulate the biological processes of various diseases and viruses. In our previous study on patients with thrombocytopenia syndrome, we conducted a longitudinal sampling study of transcriptomics and epigenetics (Nat. Commun., 2021, 12:5629). In this study, through the analysis of patient RNA-seq, we found that in patients infected with SFTSV, the expression of ADAR1 increased, and it gradually decreased with the recovery of the patients. By constructing cell models and conducting RNA sequencing analysis, we also obtained results similar to those from clinical samples. We found that ADAR1 knockdown promoted the replication of Bunyavirus (SFTSV), while overexpression inhibited virus replication. Further miRNA sequencing analysis revealed that after ADAR1 knockdown, some miRNAs with differential expression were produced, and the target genes of these differentially expressed miRNAs were closely related to neutrophil-mediated immune signaling pathways. These differentially expressed miRNAs may be due to ADAR1 editing the adenosine (A) in the double-stranded region of miRNA precursors to inosine (I), thereby changing the structure of dsRNA and making it difficult for Drosha or Dicer to obtain, thereby reducing the production of miRNAs. Considering these phenomena, we speculate that in the ADAR1 knockdown state, the changes in miRNA expression levels lead to the downregulation of genes involved in neutrophil-mediated immune signaling pathways, potentially causing neutrophil-mediated immune function impairment, thereby enhancing SFTSV replication. These findings provide new insights into the role of ADAR1 in SFTSV replication and immune signaling pathways, and provide a theoretical basis for the development of treatment strategies targeting ADAR1.

Dataset Information

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

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets