A conserved inhibitory role of suppressor of cytokine signaling 1 (SOCS1) in salmon antiviral immunity

被引:24
|
作者
Sobhkhez, Mehrdad [1 ]
Joensen, Lisbeth L. [1 ]
Tollersrud, Linn Greiner [1 ]
Strandskog, Guro [1 ]
Thim, Hanna L. [1 ]
Jorgensen, Jorunn B. [1 ]
机构
[1] UiT Arctic Univ Norway, Norwegian Coll Fishery Sci, N-9037 Tromso, Norway
来源
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY | 2017年 / 67卷
关键词
SOCS; JAK/STAT signaling; IPNV; SAV; Interferons; Atlantic salmon; PANCREATIC NECROSIS VIRUS; TROUT ONCORHYNCHUS-MYKISS; ATLANTIC SALMON; RAINBOW-TROUT; CELL-LINE; FEEDBACK INHIBITOR; GAMMA-INTERFERON; PROTEINS; ALPHAVIRUS; EXPRESSION;
D O I
10.1016/j.dci.2016.11.001
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
The SOCS proteins are regulators of JAK/STAT signaling. A number of viral infections has been associated with SOCS upregulation. Here we report that SOCS1 mRNA expression is up-regulated in salmon alphavirus (SAV3) infected TO cells, while infectious pancreatic necrosis virus infection has a negligible effect. SAV3 infected salmon showed increased SOCS1 mRNA levels in heart correlating with increased viral transcripts. Together, the in vitro and in vivo data suggests that SAV3-induced SOCS1 expression may affect the outcome of the virus infection. Using CHSE-214 cells overexpressing SOCS1 we revealed increased SAV3 replication compared to control, suggesting that SOCS1 suppress the antiviral capacity of the cells. In IFNa1-treated cells, the suppression of viral replication was partially rescued by SOCS1 overexpression. The increased viral replication in SOCS1 transgene cells was likely a result of impaired IFN-signaling and the reduced expression of interferon-stimulated genes in the transgene cells underscores this. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:66 / 76
页数:11
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