Background: Severe fever with thrombocytopenia syndrome (SFTS) was an emerging hemorrhagic fever that was caused by a tick-borne bunyavirus, SFTSV. Although SFTSV nonstructural protein can inhibit type I interferon (IFN-I) production Ex Vivo and IFN-I played key role in resistance SFTSV infection in animal model, the role of IFN-I in patients is not investigated. Methods: We have assayed the concentration of IFN-alpha, a subtype of IFN-I as well as other cytokines in the sera of SFTS patients and the healthy population with CBA (Cytometric bead array) assay. Results: The results showed that IFN-alpha, tumor necrosis factor (TNF-alpha), granulocyte colony-stimulating factor (G-CSF), interferon-gamma (IFN-gamma), macrophage inflammatory protein (MIP-1 alpha), interleukin-6 (IL-6), IL-10, interferon-inducible protein (IP-10), monocyte chemoattractant protein (MCP-1) were significantly higher in SFTS patients than in healthy persons (p < 0.05); the concentrations of IFN-alpha, IFN-gamma, G-CSF, MIP-1 alpha, IL-6, and IP-10 were significant higher in severe SFTS patients than in mild SFTS patients (p < 0.05). Conclusion: The concentration of IFN-a as well as other cytokines (IFN-gamma, G-CSF, MIP-1 alpha, IL-6, and IP-10) is correlated with the severity of SFTS, suggesting that type I interferon may not be significant in resistance SFTSV infection in humans and it may play an import role in cytokine storm.
[1]Shandong Univ, Sch Publ Hlth, Jinan 250012, Peoples R China.
[2]Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[3]Fudan Univ, Sch Med, Shanghai 200032, Peoples R China.
[4]Univ Texas Med Branch, Sch Hlth Profess, Galveston, TX 77555 USA.
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