Abstract
In March 2020, coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 was declared a global pandemic by the WHO. Obesity was rapidly identified as an independent risk factor for poor prognosis, with an increased risk of acute respiratory distress syndrome, cardiovascular and thrombo-embolic events, admission to intensive care and mortality. The white visceral adipose tissue, which increases in people suffering from obesity, appears to have a key role in this pathogenesis, as it constitutes a viral reservoir for SARS-CoV-2 through angiotensin 2-converting enzyme receptors. Following infection of host cells, activation of pro-inflammatory cytokines creates an environment suitable to the ‘cytokine storm’ and macrophage activation syndrome, associated with a risk of progression to acute respiratory distress syndrome. In obesity, the systemic spread of the virus, its entry and prolonged excretion into already inflamed adipose tissue can stimulate immune responses and the subsequent amplification of a cytokine cascade, worsening the course of the disease. The endothelial hyperactivation induced by SARS-CoV-2 combined with the state of hypofibrinolysis and endothelial dysfunction present in obesity increases the risk of thrombo-embolic events. The volume of visceral and epicardial adipose tissue measured by CT scan appears to be a good prognostic marker for these unfavorable outcomes. In addition, vaccine responses appear to be lower in these patients due to a weaker early humoral response, which means that prevention messages need to continue to be disseminated and booster vaccinations encouraged in this population. The aim of this review is to determine the role of adipose tissue in the poor prognosis of obese patients infected with SARS-CoV-2.© 2023 Société francophone nutrition clinique et métabolisme (SFNCM).Published by Elsevier Masson SAS. All rights reserved.
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