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Review
. 2018 Apr 14;10(4):196.
doi: 10.3390/v10040196.

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Yuchen Nan  1   2 , Chunyan Wu  3 , Yan-Jin Zhang  4
Affiliations
Review

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Yuchen Nan et al. Viruses. .

Abstract

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.

Keywords: Interferons; JAK/STAT signaling; inflammation; non-canonical STAT activation; viral antagonism.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic illustration of Type I, Type II, and Type III Interferon (IFN) signaling.
See this image and copyright information in PMC

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