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Viruses 2018, 10(4), 196;

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, China
Molecular Virology Laboratory, VA-MD College of Veterinary Medicine and Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20742, USA
Authors to whom correspondence should be addressed.
Received: 28 February 2018 / Revised: 7 April 2018 / Accepted: 11 April 2018 / Published: 14 April 2018
(This article belongs to the Special Issue Viruses and Inflammation)
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Interferons (IFNs) are a group of secreted proteins that play critical roles in antiviral immunity, antitumor activity, activation of cytotoxic T cells, and modulation of host immune responses. IFNs are cytokines, and bind receptors on cell surfaces to trigger signal transduction. The major signaling pathway activated by IFNs is the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway, a complex pathway involved in both viral and host survival strategies. On the one hand, viruses have evolved strategies to escape from antiviral host defenses evoked by IFN-activated JAK/STAT signaling. On the other hand, viruses have also evolved to exploit the JAK/STAT pathway to evoke activation of certain STATs that somehow promote viral pathogenesis. In this review, recent progress in our understanding of the virus-induced IFN-independent STAT signaling and its potential roles in viral induced inflammation and pathogenesis are summarized in detail, and perspectives are provided. View Full-Text
Keywords: Interferons; JAK/STAT signaling; non-canonical STAT activation; viral antagonism; inflammation Interferons; JAK/STAT signaling; non-canonical STAT activation; viral antagonism; inflammation

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Nan, Y.; Wu, C.; Zhang, Y.-J. Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation. Viruses 2018, 10, 196.

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