Host Cytokine Storm Is Associated With Disease Severity of Severe Fever With Thrombocytopenia Syndrome

被引：260

作者：

Sun, Yulan ^{[1
]}

Jin, Cong ^{[1
]}

Zhan, Faxian ^{[1
]}

Wang, Xianjun ^{[1
]}

Liang, Mifang ^{[1
]}

Zhang, Quanfu ^{[1
]}

Ding, Shujun ^{[1
]}

Guan, Xuhua ^{[1
]}

Huo, Xixiang ^{[1
]}

Li, Chuan ^{[1
]}

Qu, Jing ^{[1
]}

Wang, Qin ^{[1
]}

Zhang, Shuo ^{[1
]}

Zhang, Yanping ^{[1
]}

Wang, Shiwen ^{[1
]}

Xu, Anqiang ^{[1
]}

Bi, Zhenqiang ^{[1
]}

Li, Dexin ^{[1
]}

机构：

[1] Beijing CDC, Beijing, Peoples R China

来源：

JOURNAL OF INFECTIOUS DISEASES | 2012年 / 206卷 / 07期

关键词：

HEMORRHAGIC-FEVER; VIRUS-INFECTION; DENGUE VIRUS; BUNYAVIRUS; EXPRESSION; CHEMOKINES; PROFILES; PATTERNS; RANTES;

D O I：

10.1093/infdis/jis452

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Methods. Serum samples from 15 fatal and 44 nonfatal SFTS cases were subjected to multiplex-microbead immunoassays to detect a broad spectrum of cytokines. The viral load and virus-specific IgG titers were also tested by real-time PCR and ELISA, respectively. Results. Cytokines IL-1RA, IL-6, IL-10, G-CSF, IP-10, and MCP-1 were elevated in SFTS patients and produced at robust levels in fatal cases. In contrast, cytokines PDGF-BB and RANTES decreased in SFTS patients. These cytokines reverted to normal ranges during the convalescent phase of SFTSV infection. Cytokines IL-1 beta, IL-8, MIP-1 alpha, and MIP-1 beta showed a unique pattern of elevation in fatal cases but not in nonfatal cases. However, these cytokines increased in the convalescent phase of nonfatal SFTS cases. Our regression analysis revealed that the serum viral load correlated with these cytokines. Moreover, levels of these cytokines correlated with various clinical parameters and virus-specific IgG titers. Conclusion. The study demonstrates that SFTSV infection induces a cytokine storm with abnormally expressed cytokine profiles, which are associated with the disease severity.

引用

页码：1085 / 1094

页数：10

共 28 条

[1] NSs protein of rift valley fever virus blocks interferon production by inhibiting host gene transcription [J].