Antioxidant, anti-inflammatory and immunomodulatory roles of vitamins in COVID-19 therapy

oxidative stress is caused by an abundant generation of reactive oxygen species, associated to a diminished capacity of the endogenous systems of the organism to counteract them. Activation of pro-oxidative pathways and boosting of inflammatory cytokines are always encountered in viral infections, including SARS-CoV-2. So, the importance of counteracting cytokine storm in COVID-19 pathology is highly important, to hamper the immunogenic damage of the endothelium and alveolar membranes. Antioxidants prevent oxidative processes, by impeding radical species generation. It has been proved that vitamin intake lowers oxidative stress markers, alleviates cytokine storm and has a potential role in reducing disease severity, by lowering pro-inflammatory cytokines, hampering hyperinflammation and organ failure. For the approached compounds, direct antiviral roles are also discussed in this review, as these activities encompass secretion of antiviral peptides, modulation of angiotensin-converting enzyme 2 receptor expression and interaction with spike protein, inactivation of furin protease, or inhibition of pathogen replication by nucleic acid impairment induction. Vitamin administration results in beneficial effects. Nevertheless, timing, dosage and mutual influences of these micronutrients should be carefullly regarded. (c) 2022 Elsevier Masson SAS. All rights reserved.

Automated summary

Oxidative stress is caused by an abundant generation of reactive oxygen species and a diminished capacity of the organism's endogenous systems to counteract them. In viral infections, activation of pro-oxidative pathways and increased inflammatory cytokines are common. Vitamin intake has been shown to lower oxidative stress markers, alleviate cytokine storm, and potentially reduce disease severity. Antioxidants also play a role in directly combating the virus. Careful consideration of timing, dosage, and interactions of micronutrients is important.