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      Interferon Gamma Inhibits Equine Herpesvirus 1 Replication in a Cell Line-Dependent Manner

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          Abstract

          The sole equine herpesvirus 1 (EHV-1) immediate-early protein (IEP) is essential for viral replication by transactivating viral immediate-early (IE), early (E), and late (L) genes. Here, we report that treatment of mouse MH-S, equine NBL6, and human MRC-5 cells with 20 ng/mL of IFN-γ reduced EHV-1 yield by 1122-, 631-, and 10,000-fold, respectively. However, IFN-γ reduced virus yield by only 2–4-fold in mouse MLE12, mouse L-M, and human MeWo cells compared to those of untreated cells. In luciferase assays with the promoter of the EHV-1 early regulatory EICP0 gene, IFN-γ abrogated trans-activation activity of the IEP by 96% in MH-S cells, but only by 21% in L-M cells. Similar results were obtained in assays with the early regulatory UL5 and IR4 promoter reporter plasmids. IFN-γ treatment reduced IEP protein expression by greater than 99% in MH-S cells, but only by 43% in L-M cells. The expression of IEP and UL5P suppressed by IFN-γ was restored by JAK inhibitor treatment, indicating that the inhibition of EHV-1 replication is mediated by JAK/STAT1 signaling. These results suggest that IFN-γ blocks EHV-1 replication by inhibiting the production of the IEP in a cell line-dependent manner. Affymetrix microarray analyses of IFN-γ-treated MH-S and L-M cells revealed that five antiviral ISGs (MX1, SAMHD1, IFIT2, NAMPT, TREX1, and DDX60) were upregulated 3.2–18.1-fold only in MH-S cells.

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          Mechanisms of type-I- and type-II-interferon-mediated signalling.

          Interferons are cytokines that have antiviral, antiproliferative and immunomodulatory effects. Because of these important properties, in the past two decades, major research efforts have been undertaken to understand the signalling mechanisms through which these cytokines induce their effects. Since the original discovery of the classical JAK (Janus activated kinase)-STAT (signal transducer and activator of transcription) pathway of signalling, it has become clear that the coordination and cooperation of multiple distinct signalling cascades - including the mitogen-activated protein kinase p38 cascade and the phosphatidylinositol 3-kinase cascade - are required for the generation of responses to interferons. It is anticipated that an increased understanding of the contributions of these recently identified pathways will advance our current thinking about how interferons work.
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            Evolution has resorted to nitric oxide (NO), a tiny, reactive radical gas, to mediate both servoregulatory and cytotoxic functions. This article reviews how different forms of nitric oxide synthase help confer specificity and diversity on the effects of this remarkable signaling molecule.
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              Interferon-stimulated genes and their antiviral effector functions

              Highlights ► IFN induces a diverse range of antiviral effectors. ► Each virus has a unique, but partially overlapping, antiviral ‘ISG profile’. ► IFN effectors target multiple stages in the virus life cycle. ► The IFN signaling pathway is highly self-reinforcing. ► Viruses may hijack IFN effectors to promote replication.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Pathogens
                Pathogens
                pathogens
                Pathogens
                MDPI
                2076-0817
                16 April 2021
                April 2021
                : 10
                : 4
                : 484
                Affiliations
                Center for Molecular and Tumor Virology, Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA 71130-3932, USA; shakyaakhilesh@ 123456gmail.com (A.K.S.); docall@ 123456lsuhsc.edu (D.J.O.)
                Author notes
                [* ]Correspondence: skim1@ 123456lsuhsc.edu ; Tel.: +1-318-675-4505; Fax: +1-318-675-5764
                Article
                pathogens-10-00484
                10.3390/pathogens10040484
                8073143
                33923733
                de93ad15-8392-4a2b-b80d-755f615fd46d
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 13 March 2021
                : 13 April 2021
                Categories
                Article

                equine herpesvirus 1,iep,interferon gamma,jak/stat1 signaling,interferon-stimulated genes,microarray

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