PMC:7128678 / 2199-3603 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7128678","sourcedb":"PMC","sourceid":"7128678","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7128678","text":"The recent emergence of the novel pathogenic SARS-coronavirus 2 (SARS-CoV-2) is responsible for a global pandemic [1], and there is an urgent need to identify active antiviral agents. Given the global health emergency, drug repositioning is the most reliable option to design an efficient therapy for infected patients without delay [2,3]. Several drugs have already been tested, among which chloroquine (CLQ), a well-known antimalarial drug, is one of the most promising as it has shown apparent efficacy in the treatment of COVID-19-associated pneumonia in recent clinical studies [4]. However, the mechanism of action of CLQ against SARS-CoV-2 is unclear as the drug seems to exert a broad range of potential antiviral effects [5]. Therefore, although CLQ is classically considered as an inhibitor of endocytic pathways through elevation of endosomal pH [6], its detailed molecular mechanism of action as an antiviral compound remains unclear [3,5]. Interestingly, CLQ has been shown to interfere with the terminal glycosylation of angiotensin-converting enzyme-2 (ACE-2) [7], which acts as a plasma membrane receptor for both SARS-CoV [8] and SARS-CoV-2 [9], and CLQ could act at several steps of the coronavirus replication cycle [7]. These data suggest the interesting and mostly unexplored possibility that CLQ could prevent viral attachment through a direct effect on host cell surface 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