College of Agriculture & Natural Resources

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The collections in this community comprise faculty research works, as well as graduate theses and dissertations.

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    Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation
    (MDPI, 2018-04-14) Nan, Yuchen; Wu, Chunyan; Zhang, Yan-Jin
    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.
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    Interferense of Host Innate Immune Response by Hepatitis E Virus
    (2014) Nan, Yuchen; Zhang, Yanjin; Veterinary Medical Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    The host antiviral innate immunity mainly relies on host pattern recognition receptors (PRR) and downstream interferon (IFN) signaling. Host PRR for RNA viruses include Toll-like receptors (TLR) and Retinoic acid-inducible gene I (RIG-I) like receptors (RLR). Activation of both TLR and RLR pathways can eventually lead to the secretion of type I IFNs, which can modulate both innate and adaptive immune responses against viral pathogens, including hepatitis E virus (HEV). HEV causes acute hepatitis in humans and has been responsible for several outbreaks of hepatitis across the world. Currently, no commercial vaccine is available for the prevention of HEV infection in any country except China. HEV biology and pathogenesis as well as its responses to host innate immunity are poorly understood, though other hepatitis viruses, including the hepatitis A, B and C viruses, have been much better studied. In this study, how HEV interferes with IFN induction and IFN-activated signaling had been examined. Results showed that the protein encoded by HEV ORF1 can inhibit type I IFN synthesis and downstream JAK/STAT signaling pathway. However, the HEV ORF3 product is able to enhance RIG-I-mediated signaling to a certain extent. These data suggest that HEV proteins interfere with the host innate immune response and may exert the diverse roles depending on the stage and/or context of infection. These studies contribute to a better understanding of HEV pathogenesis and may facilitate a strategy development for the prevention and control of HEV infection.