Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections

被引:115
作者
Okabayashi, T
Kariwa, H
Yokota, S
Iki, S
Indoh, T
Yokosawa, N
Takashima, I
Tsutsumi, H
Fujii, N
机构
[1] Sapporo Med Univ, Sch Med, Dept Microbiol, Chuo Ku, Sapporo, Hokkaido 0608556, Japan
[2] Hokkaido Univ, Grad Sch Vet Med, Dept Environm Vet Sci, Publ Hlth Lab, Sapporo, Hokkaido 060, Japan
[3] Hokkaido Univ, Sch Med, Dept Pediat, Sapporo, Hokkaido 060, Japan
关键词
SARS-CoV; SOCS3; cytokine; IL-6; IFN; TLR;
D O I
10.1002/jmv.20556
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS-CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS-CoV infection. Therefore, SARS-CoV replication was suppressed by pretreatment with IFN. SARS-CoV and RSV induced high levels of IL-6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling-3 (SOCS3) by SARS-CoV was significantly lower than that by RSV in spite of the significant production of IL-6. Toll-like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS-CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with "severe" inflammation in SARS.
引用
收藏
页码:417 / 424
页数:8
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