| BRIEF REPORT |
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| Year : 2020 | Volume
: 4
| Issue : 3 | Page : 189-192 |
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Macrolides and COVID-19: An optimum premise
Hayder M Al-Kuraishy1, Marwa S Al-Naimi1, Claire M Lungnier2, Ali I Al-Gareeb1
1 Department of Clinical Pharmacology, Medicine and Therapeutic, Faculty of Medical, College of Medicine, Al-Mustansiriya University, Baghdad, Iraq
2 Mitochondria, Oxidative Stress and Muscular Protection, Institute of Physiology, Faculty of Medicine, Directeur de Recherche I CNRS Emérite, Strasbourg, France
Correspondence Address:
Prof. Hayder M Al-Kuraishy
Department of Clinical Pharmacology, Medicine and Therapeutic, Faculty of Medical, College of Medicine, Al-Mustansiriya University, Baghdad
Iraq
 Source of Support: None, Conflict of Interest: None  | 2 |
DOI: 10.4103/bbrj.bbrj_103_20
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The epidemic of coronavirus infection disease 19 (COVID-19), which started in Wuhan City, is caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2) which binds angiotensin-converting enzyme 2 (ACE2) receptor, which is highly expressed by the lung epithelial cells. In COVID-19-induced acute respiratory distress syndrome, a hyperinflammatory syndrome with hypercytokinemia leads to acute lung injury and the development of respiratory failure. Macrolides are broad-spectrum, bacteriostatic antibiotics with significant anti-inflammatory and immunomodulatory effects. Different preclinical and clinical studies have shown that macrolides inhibit cytokine release, attenuate the inflammatory response, and improve immunoglobulin response. Azithromycin potentiates the anti-SARS-CoV-2 activity of chloroquine in COVID-19. However, azithromycin alone is effective initially in the management of COVID-19 due to its antiviral and anti-inflammatory activity. The antiviral potential of azithromycin is linked to different mechanisms, including modulation of lysosomal activity and the interaction points between SARS-CoV-2 and ACE2 receptor. Therefore, macrolides, chiefly azithromycin, are an effective drug against COVID-19 through direct antiviral effect or via the modulation of hyperinflammatory status.
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