Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5540209 | Developmental & Comparative Immunology | 2017 | 30 Pages |
Abstract
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.
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Authors
Mehrdad Sobhkhez, Lisbeth L. Joensen, Linn Greiner Tollersrud, Guro Strandskog, Hanna L. Thim, Jorunn B. Jørgensen,