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J Med Virol. 2020 Apr 15. doi: 10.1002/jmv.25887. [Epub ahead of print]
Hyperglycemia, Hydroxychloroquine, and the COVID-19 Epidemic.
Brufsky A1.
Author information
Abstract
COVID-19 infection and its severity can be explained by the concentration of glycosylated SARS- CoV-2 viral particles in the lung epithelium, the concentration of glycosylated angiotensin converting enzyme receptor 2 (ACE2) in the lung epithelium, and the degree and control of the pulmonary immune response to the SARS-CoV-2 spike protein at approximately day 8-10 after symptom onset, which may be related to both. Binding of ACE2 by SARS-CoV-2 in COVID-19 also suggests that prolonged uncontrolled hyperglycemia, and not just a history of diabetes mellitus, may be important in the pathogenesis of the disease. It is tempting to consider that the same mechanism acts in COVID-19 as in SARS, where an overactive macrophage M1 inflammatory response, as neutralizing antibodies to the SARS-CoV- 2 spike protein form at day 7-10, results in acute respiratory distress syndrome (ARDS) in susceptible patients. It is also allows consideration of agents, such as hydroxychloroquine, which may interfere with this overly brisk macrophage inflammatory response and perhaps influence the course of the disease, in particular those that blunt but do not completely abrogate the M1 to M2 balance in macrophage polarization, as well as viral load, which in SARS appears to be temporally related to the onset of ARDS. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
SARS coronavirus; antibody-mediated cell-mediated cytotoxicity; antiviral agents
PMID:32293710DOI:10.1002/jmv.25887