A recent review investigated Zinc impact on COVID-19. Zinc is known to regulate inflammatory response and modulate antiviral and antibacterial immunity. Despite the paucity of clinical data, certain indications advocate that zinc status modulation may be valuable in COVID-19. Numerous in-vitro experiments indicate that Zn2+ possesses antiviral activity via SARS-CoV RNA polymerase inhibition.

This effect might form the basis of chloroquine's therapeutic potency that is known to act as zinc ionophore. Indirect evidence also denotes that Zn2+ may diminish ACE2 (angiotensin-converting enzyme 2) activity, which is known to be the SARS-CoV-2 receptor. Enhanced antiviral immunity by zinc may also occur by up-regulating the production of interferon-α and elevating its antiviral effect.

Zinc also has anti-inflammatory activity by inhibiting NF-κB signaling and modulation of regulatory T-cell functions that might mitigate the cytokine storm in COVID-19. By upgrading barrier function and mucociliary clearance of respiratory epithelium, as well as by direct antibacterial activity against S.pneumoniae, improved Zn status may also diminish bacterial co-infection risk.

Zinc status is also notably related to risk factors for severe COVID-19 pandemic (aging, obesity, atherosclerosis, immune deficiency, and diabetes) since these are zinc deficiency known risk groups. Therefore, Zn may demonstrate protective effect as preventive and adjuvant therapy of COVID-19 through mucociliary clearance improvement, ventilator-induced lung injury prevention, modulation of antibacterial and antiviral immunity, and diminishing inflammation.

However, there is a requisition of further clinical and experimental studies to elucidate the potential role of Zn deficiency in COVID-19 susceptibility, as well as the effects of Zn supplementation, and the underlying mechanisms.