Obesity and SARS-CoV-2 Infection a Multifaceted Interplay - Adipose Tissue Inflammation, Adipokine Disbalance and Immunity

Abstract

Overweight and obesity are the most common comorbidities in SARSCoV- 2 patients, requiring hospitalization in intensive care units. The multifaceted nature of obesity including its effects on respiratory mechanics and immunity can fundamentally alter the pathogenesis of acute respiratory distress syndrome and pneumonia, which are the major causes of death due to SARS-CoV-2 infection. Most coronaviruses overcome host antiviral defense, and the pathogenicity of the virus is related to its capacity to suppress host immunity. Hyperleptinemia, insulin resistance and adipose tissue inflammation are hallmarks of obesity, which is associated with a leptin and insulin resistant state. Leptin regulates appetite and metabolism and through the Jak/STAT and Akt pathways modulates T cell number and function; insulin receptor signaling is closely engaged in T cell proliferation, whereas low garde adipose tissue inflammation provokes aberrant inflammasome activation. The review discusses these phenomena. It presents the reasons for susceptibility to respiratory viral infections in obese patients, as well as, the immunomodulatory effects of obesity to the outcome.