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To the Editor: 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 metabolicassociated fatty liver disease (MAFLD).1 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.2 Despite this retrospective study, there is growing evidence that patients with MAFLD are at higher risk of COVID19 disease progression.3–5
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