Could targeting immunometabolism be a way to control the burden of COVID-19 infection?

Abstract

This review portrays the metabolic consequences of Covid-19 infection at different stages of the clinical syndrome. It also describes how events can change when patients with metabolic problems are infected and the effects that diet and nutrition might play to influence the outcome of infection. We also discuss the types of maneuvers that could be used to reshape metabolic events and question if this approach could be a practical therapy used alone or in combination with other approaches to reduce the burden of Covid-19 infection.

Keywords: Anti-metabolite therapy; Covid-19; Immunometabolism; Metabolic disease; Nutrition; SARS-Cov-2.

Fig. 1

Schematic representation of some changes in cellular metabolism attributed to Covid-19 infection. ACE2; angiotensin-converting enzyme 2 and TMPRSS2; transmembrane protease serine 2 [6], FAS; fatty acid synthesis [15], IDO; indoleamine 2,3-dioxygenase [15,16], HIF-1α; hypoxia inducible factor 1 subunit alpha [18,19], ROS; reactive oxygen species [19], PPARγ; peroxisome proliferator-activated receptor gamma [20].

Fig. 2

Cellular metabolism map showing pathways that could be targeted with metabolic drugs and inhibitors to reduce the burden of infection. Mitoquinol; ROS (reactive oxygen species) inhibitor [19], BAY87; HIF-1α (hypoxia inducible factor 1 alpha) inhibitor [19], 2DG (2-Deoxy-d-glucose); inhibits glycolysis [19,23], fenofibrate; reduce lipid level and accumulation [24], statin; HMG-CoA reductase (3-hydroxy-3-methyl-glutaryl-CoA) inhibitor [73], PF-05175157; acetyl-CoA carboxylase 1 and 2 inhibitor [78], DON (6-Diazo-5-oxo-l-norleucine); inhibits glutaminolysis [79], metformin; ETC (electron transport chain) complex I inhibitor [85], TCA; tricarboxylic acid cycle, FAS; fatty acid synthesis.