The release of NETs during SFTSV infection downregulates the specific inflammatory factors that lead to liver and spleen damage.

Abstract

Severe fever with thrombocytopenia syndrome is a life-threatening condition that has been the focus of attention in recent years. It is primarily caused by uncontrolled replication of a novel Bunyavirus and an intense pro-inflammatory response. NETosis is a form of cell death initiated by neutrophils, involving the formation of neutrophil extracellular traps. These NETs are composed of DNA fibers or nuclear chromatin that trap cytoplasmic granule proteins and histones in a meshwork to capture and eliminate pathogens.Our investigation delved into single-cell sequencing data from SFTS patients, revealing that SFTSV can trigger NETosis in both cellular and animal models. Furthermore, we examined the impact of NETs on Thp-1 cells through transcriptome sequencing and evaluated tissues in infected animal models, unveiling a significant down-regulation of specific inflammatory factors. By integrating previous research, we propose a hypothesis that the reduction of these inflammatory factors hinders the occurrence of immune responses and the process of organ repair, thereby causing tissue damage.