Zinc and respiratory tract infections: Perspectives for COVID‑19 (Review)

In view of the emerging COVID19 pandemic caused by SARSCoV2 virus, the search for potential protective and therapeutic antiviral strategies is of particular and urgent interest. Zinc is known to modulate antiviral and antibacterial immunity and regulate inflammatory response. Despite the lack of clinical data, certain indications suggest that modulation of zinc status may be beneficial in COVID19. In vitro experiments demonstrate that Zn2+ possesses antiviral activity through inhibition of SARSCoV RNA polymerase. This effect may underlie therapeutic efficiency of chloroquine known to act as zinc ionophore. Indirect evidence also indicates that Zn2+ may decrease the activity of angiotensinconverting enzyme 2 (ACE2), known to be the receptor for SARSCoV2. Improved antiviral immunity by zinc may also occur through upregulation of interferon alpha production and increasing its antiviral activity. Zinc possesses antiinflammatory activity by inhibiting NFkappaB signaling and modulation of regulatory Tcell functions that may limit the cytokine storm in COVID19. Improved Zn status may also reduce the risk of bacterial coinfection by improving mucociliary clearance and barrier function of the respiratory epithelium, as well as direct antibacterial effects against S. pneumoniae. Zinc status is also tightly associated with risk factors for severe COVID19 including ageing, immune deficiency, obesity, diabetes, and atherosclerosis, since these are known risk groups for zinc deficiency. Therefore, Zn may possess protective effect as preventive and adjuvant therapy of COVID19 through reducing inflammation, improvement of mucociliary clearance, prevention of ventilatorinduced lung injury, modulation of antiviral and antibacterial immunity. However, further clinical and experimental studies are required.