The world is currently facing a frightening coronavirus disease-2019 (COVID-19) epidemic. Severity of COVID-19 presentation is highly variable among infected individuals with increasingly recognized risk factors. Although observational studies suggested lower COVID-19 severity in populations consuming fermented foods, no controlled study investigated the role of diet. Yogurt, a fermented dairy product, exhibits interesting properties related to the presence of bioactive peptides and probiotics that may play a beneficial role in COVID-19 presentation and outcome. Peptides contained in yogurt are responsible for angiotensin-converting enzyme-inhibitory, bradykinin potentiating, antiviral, anti-inflammatory, antithrombotic, and antioxidant effects. The types and activity of these peptides vary widely depending on their amino acid sequence, on the probiotics used in yogurt production and on intestinal digestion. Additionally, probiotics used in yogurt exhibit direct angiotensin-converting enzyme-inhibitory, antiviral and immune boosting activities. Since COVID-19 pathogenesis involves angiotensin II accumulation and bradykinin deficiency, yogurt bioactive peptides appear as potentially beneficial. Therefore, epidemiological investigations and randomized controlled clinical trials to evaluate the exact role of yogurt consumption on COVID-19 manifestations and outcome should be encouraged.

Hypozincemia is prevalent in severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)-infected patients and has been considered as a risk factor in severe coronavirus disease-2019 (COVID-19). Whereas zinc might affect SARS-COV-2 replication and cell entry, the link between zinc deficiency and COVID-19 severity could also be attributed to the effects of COVID-19 on the body metabolism and immune response. Zinc deficiency is more prevalent in the elderly and patients with underlying chronic diseases, with established deleterious consequences such as the increased risk of respiratory infection. We reviewed the expected effects of zinc deficiency on COVID-19-related pathophysiological mechanisms focusing on both the renin–angiotensin and kinin-kallikrein systems. Mechanisms and effects were extrapolated from the available scientific literature. Zinc deficiency alters angiotensin-converting enzyme-2 (ACE2) function, leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, which results in an exaggerated pro-inflammatory response, vasoconstriction and pro-thrombotic effects. Additionally, zinc deficiency blocks the activation of the plasma contact system, a protease cascade initiated by factor VII activation. Suggested mechanisms include the inhibition of Factor XII activation and limitation of high-molecular-weight kininogen, prekallikrein and Factor XII to bind to endothelial cells. The subsequent accumulation of Factor XII and deficiency in bradykinin are responsible for increased production of inflammatory mediators and marked hypercoagulability, as typically observed in COVID-19 patients. To conclude, zinc deficiency may affect both the renin–angiotensin and kinin-kallikrein systems, leading to the exaggerated inflammatory manifestations characteristic of severe COVID-19.