Abstract
Signal transducer and activator of transcription 3 (STAT3) is a key regulator of numerous physiological functions, including the immune response. As pathogens elicit an acute phase response with concerted activation of STAT3, they are confronted with two evolutionary options: either curtail it or employ it. This has important consequences for the host, since abnormal STAT3 function is associated with cancer development and other diseases. This review provides a comprehensive outline of how human viruses cope with STAT3-mediated inflammation and how this affects the host. Finally, we discuss STAT3 as a potential target for antiviral therapy.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Humans
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Inflammation / etiology*
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Inflammation / metabolism
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Inflammation / pathology
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STAT3 Transcription Factor / metabolism*
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Signal Transduction
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Virus Diseases / metabolism
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Virus Diseases / virology*
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Viruses / pathogenicity*
Substances
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STAT3 Transcription Factor
Grants and funding
This work was supported by grants from the Wilhelm Sander-Stiftung (Förderantrag 2010.023.1 to TFB -
www.wilhelm-sander-stiftung.de), the European Union (Interreg IV-Rhin Supérieur-FEDER-Hepato-Regio-Net to TFB -
www.interreg-rhin-sup.eu; ERC-AdG-2014 HEPCIR to TFB -
www.cordis.europa.eu/project/rcn/198487_en.html; EU H2020 HEPCAR to TFB -
www.hep-car.eu), the French Cancer Agency (ARC IHU201301187 to TFB -
www.fondation-arc.org), the University of Strasbourg (IdEx, Projet Attractivité 2014, ANR, to JL -
www.en.unistra.fr), the French ANRS (ECTZ4236, ECTZ4446 to JL and AARS -
www.anrs.fr) and Cancéropôle Est (AAP Emergence du CGE / 2017 to JL, -
www.canceropole-ge.org). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.