Do nutrients and other bioactive molecules from foods have anything to say in the treatment against COVID-19?

Abstract

The repositioning of therapeutic agents already approved by the regulatory agencies for the use of drugs is very interesting due to the immediacy of their use; similarly, the possibility of using molecules derived from foods, whether nutrients or not, is of great importance, also because of their immediate therapeutic applicability. Candidates for these natural therapies against COVID-19 should show certain effects, such as restoring mitochondrial function and cellular redox balance. This would allow reducing the susceptibility of risk groups and the cascade of events after SARS-CoV-2 infection, responsible for the clinical picture, triggered by the imbalance towards oxidation, inflammation, and cytokine storm. Possible strategies to follow through the use of substances of food origin would include: a) the promotion of mitophagy to remove dysfunctional mitochondria originating from free radicals, proton imbalance and virus evasion of the immune system; b) the administration of transition metals whose redox activity would lead to their own oxidation and the consequent generation of a reduced environment, which would normalize the oxidative state and the intracellular pH; c) the administration of molecules with demonstrated antioxidant capacity; d) the administration of compounds with anti-inflammatory and vasodilatory activity; e) the administration of immunomodulatory compounds.

Keywords: Curcumin; Polyphenols; Vitamin C; Vitamin D; Zinc.

Fig. 1

SARS-CoV-2 and its interaction with the Renin Angiotensin Aldosterone System (RAS). ACE2 degrades angiotensin I to angiotensin (1–9), which is a ligand for angiotensin II receptor type 2 (AT2R). ACE2 also converts angiotensin II to angiotensin (1–7) that binds to the Mas receptor (MASR). Angiotensin (1–9) has regenerative and anti-inflammatory effects, angiotensin (1–7) mediates anti-inflammatory and vasodilatory effects and reduces reactive oxygen species (ROS) through its binding to AT2R. Thus, angiotensin (1–7) and angiotensin (1–9) counteract the vasoconstriction and pro-inflammatory effects of angiotensin II preventing tissue injuries. SARS-CoV-2 infection would reduce ACE2 expression dysregulating RAS protective pathways.

Fig. 2

Internalization and viral replication. The process of entry of SARS-CoV-2 into the cell needs the binding of glycoprotein S to angiotensin-converting enzyme 2 (ACE2) (present in lungs but also in the kidneys, heart, gastrointestinal tract, and other sites), which act as a receptor. Type II transmembrane serine protease (TMPRSS2) present on the surface of the host cell would remove ACE2-activated receptor-like spike S proteins inducing changes that allows the virus to enter the cell. Once inside the cell, SARS-CoV-2 will translate its genetic material into the nucleus after liberation into the cytoplasm.