Fig. 1: Mechanisms linking obesity, characterized by a state of low-grade inflammation, to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

SARS-CoV-2 pathophysiology includes firstly a cellular tropism versus adipocytes that express a high level of angiotensin-converting enzyme 2 (ACE2), type 2 transmembrane serine protease (TMPRSS2), and transmembrane glycoprotein receptor (CD147). The dysregulation of the immune response by SARS-CoV-2 is characterized by the so-called “cytokine storm” with the increase in interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), interleukin-1β (IL-1β), ferritin and C-reactive protein (CRP) levels, number of macrophages, and the decrease in number of lymphocytes. In turn, low-grade inflammation, the impaired immune system with the increase in IL-6, TNFα, IL-1β, macrophages, leptin, cytotoxic T cells (CD8 + ) and the decrease in adiponectin and regulatory T cells (CD4 + ). Both the diseases impair lipid metabolism with the increase in free fatty acids (FFA) and are potentially trigger of fat embolism syndrome (FES). Hypercoagulopathy, endothelial cell damage and thrombo-inflammation with increase in plasminogen activator inhibitor 1 (PAI-1) and hypoxia-induced factor (HIF)-α levels was described in both obesity and the coronavirus 19 disease (CoVID-19) and are linked to the dysregulation of the immune system. Finally, the dysregulation of the renin–angiotensin–aldosterone system (RAAS) is another common element between the two pathologies. All these mechanisms appear to interact to each other to induce a worst prognosis in CoVID-19 patients with obesity.