CD8+ T cells mediate antiviral response in severe fever with thrombocytopenia syndrome

Severe fever with thrombocytopenia syndrome (SFTS), which is caused by a novel Bunyavirus, has gradually become a threatening infectious disease in rural areas of Asia. Studies have identified a severe cytokine storm and impaired humoral immune response in SFTS. However, the cellular immune response to SFTS virus (SFTSV) infection remains largely unknown. Here we report that SFTS patients had a cytokine storm accompanied by high levels of chemokines. CD8(+) T cells in peripheral blood mononuclear cells of SFTS patients exhibited a more activated phenotype and enhanced the antiviral responses. They increased the expression of CD69 and CD25, secreted a higher level of IFN-gamma and granzyme, and had a stronger proliferative ability than in healthy controls. In convalescent SFTS patients, the expression of CD69 and CD25 on CD8(+) T cells was reduced. In addition, we found the ratio and cellularity of CD14(+)CD16(+) intermediate monocytes were increased in peripheral blood of SFTS patients. Both the expression of C-X-C motif chemokine ligand 10 (CXCL10) on CD14(+)CD16(+) intermediate monocytes and the expression of C-X-C motif chemokine receptor 3 (CXCR3) on CD8(+) T cells increased dramatically in SFTS patients. Our studies reveal a potential pathway that CD8(+) T cells rapidly activate and are mostly recruited by intermediate monocytes through CXCL10 in SFTSV infection. Our results may be of clinical relevance for further treatment and discharge instructions in SFTSV infections.

Automated summary

SFTS is a threatening infectious disease caused by a novel Bunyavirus. SFTS patients exhibit a cytokine storm and impaired immune response, but their cellular immune response remains largely unknown.