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Obese patients with NASH have increased hepatic expression of SARS-CoV-2 critical entry points

  • Author Footnotes
    † Contributed equally.
    Marcos F. Fondevila
    Footnotes
    † Contributed equally.
    Affiliations
    Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain

    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain
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  • Author Footnotes
    † Contributed equally.
    Maria Mercado-Gómez
    Footnotes
    † Contributed equally.
    Affiliations
    Liver Disease Laboratory, Center for Cooperative Research in Biosciences (CIC bioGUNE, Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, and CIBER de Enfermedades Hepaticas y Digestivas (CIBERehd), Spain
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  • Author Footnotes
    † Contributed equally.
    Amaia Rodríguez
    Footnotes
    † Contributed equally.
    Affiliations
    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain

    Obesity Area, Clínica Universidad de Navarra and IdiSNA, Pamplona, Spain
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  • Author Footnotes
    † Contributed equally.
    Maria J. Gonzalez-Rellan
    Footnotes
    † Contributed equally.
    Affiliations
    Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain

    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain
    Search for articles by this author
  • Paula Iruzubieta
    Affiliations
    Department of Gastroenterology and Hepatology, Marqués de Valdecilla University Hospital, Research Institute Marqués de Valdecilla (IDIVAL), Santander, Spain
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  • Víctor Valentí
    Affiliations
    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain

    Obesity Area, Clínica Universidad de Navarra and IdiSNA, Pamplona, Spain
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  • Javier Escalada
    Affiliations
    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain

    Obesity Area, Clínica Universidad de Navarra and IdiSNA, Pamplona, Spain
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  • Markus Schwaninger
    Affiliations
    Institute for Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Lübeck, Germany
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  • Vincent Prevot
    Affiliations
    Univ. Lille, Inserm, CHU Lille, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Lille Neuroscience & Cognition, UMR-S 1172, European Genomic Institute for Diabetes (EGID), F-59000 Lille, France
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  • Carlos Dieguez
    Affiliations
    Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain

    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain
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  • Javier Crespo
    Affiliations
    Department of Gastroenterology and Hepatology, Marqués de Valdecilla University Hospital, Research Institute Marqués de Valdecilla (IDIVAL), Santander, Spain
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  • Gema Frühbeck
    Affiliations
    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain

    Obesity Area, Clínica Universidad de Navarra and IdiSNA, Pamplona, Spain
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  • Maria L. Martinez-Chantar
    Correspondence
    Corresponding authors. Addresses: Liver Disease Laboratory, Center for Cooperative Research in Biosciences (CIC bioGUNE, Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, Spain (M.L. Martinez-Chantar) or
    Affiliations
    Liver Disease Laboratory, Center for Cooperative Research in Biosciences (CIC bioGUNE, Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160 Derio, and CIBER de Enfermedades Hepaticas y Digestivas (CIBERehd), Spain
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  • Ruben Nogueiras
    Correspondence
    Department of Physiology, Research Centre of Molecular Medicine and Chronic Diseases (CIMUS), Instituto de Investigación Sanitaria de Santiago de Compostela, Universidad de Santiago de Compostela (USC), Santiago de Compostela, Spain (R. Nogueiras).
    Affiliations
    Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain

    CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain

    Galician Agency of Innovation (GAIN), Santiago de Compostela, Spain
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  • Author Footnotes
    † Contributed equally.
Published:October 19, 2020DOI:https://doi.org/10.1016/j.jhep.2020.09.027
      We read with great interest the article published by Biquard and colleagues showing that, according to public transcriptomic data, the hepatic expression of angiotensin converting enzyme 2 (ACE2) and the cellular transmembrane protease serine 2 (TMPRSS2) remains unchanged in patients with metabolic-associated fatty liver disease (MAFLD).
      • Biquard L.
      • Valla D.
      • Rautou P.E.
      No evidence for an increased liver uptake of SARS-CoV-2 in metabolic-associated fatty liver disease.
      SARS-CoV-2 attaches to cells by binding to its receptor ACE2. TMPRSS2 then cleaves the SARS-CoV-2 spike protein, allowing fusion of cellular and viral membranes.
      • Hoffmann M.
      • Kleine-Weber H.
      • Schroeder S.
      • Kruger N.
      • Herrler T.
      • Erichsen S.
      • et al.
      SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor.
      Despite this retrospective study, there is growing evidence that patients with MAFLD are at higher risk of COVID-19 disease progression.
      • Ji D.
      • Qin E.
      • Xu J.
      • Zhang D.
      • Cheng G.
      • Wang Y.
      • et al.
      Non-alcoholic fatty liver diseases in patients with COVID-19: a retrospective study.
      • Zhou Y.J.
      • Zheng K.I.
      • Wang X.B.
      • Yan H.D.
      • Sun Q.F.
      • Pan K.H.
      • et al.
      Younger patients with MAFLD are at increased risk of severe COVID-19 illness: a multicenter preliminary analysis.
      • Zhou Y.J.
      • Zheng K.I.
      • Wang X.B.
      • Sun Q.F.
      • Pan K.H.
      • Wang T.Y.
      • et al.
      Metabolic-associated fatty liver disease is associated with severity of COVID-19.
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      Linked Article

      • No evidence for an increased liver uptake of SARS-CoV-2 in metabolic-associated fatty liver disease
        Journal of HepatologyVol. 73Issue 3
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          We read with interest the research article published by Ji and colleagues, in the Journal of Hepatology, showing that patients with metabolic-associated fatty liver disease (MAFLD) have a higher risk of COVID-19 disease progression and higher likelihood of abnormal liver blood tests from admission to discharge than patients without MAFLD.1 Given the absence of data on medical history of these patients, this persistence of liver blood test abnormalities could be either a mere reflection of pre-existing abnormalities related to MAFLD or could alternatively be due to a higher susceptibility of the fatty liver to SARS-CoV-2 infection.
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