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

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 proinflammatory response. NETosis is a form of cell death initiated by neutrophils, involving the formation of neutrophil extracellular traps. These neutrophil extracellular traps 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 patients with severe fever with thrombocytopenia syndrome, revealing that severe fever with thrombocytopenia syndrome virus can trigger NETosis in both cellular and animal models. Furthermore, we examined the impact of neutrophil extracellular traps on Thp-1 cells through transcriptome sequencing and evaluated tissues in infected animal models, unveiling a significant downregulation 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.