Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged in December 2019 and rapidly outspread worldwide endangering human health. The coronavirus disease 2019 (COVID-19) manifests itself through a wide spectrum of symptoms that can evolve to severe presentations as pneumonia and several non-respiratory complications. Increased susceptibility to COVID-19 hospitalization and mortality have been linked to associated comorbidities as diabetes, hypertension, cardiovascular diseases and, recently, to obesity. Similarly, individuals living with obesity are at greater risk to develop clinical complications and to have poor prognosis in severe influenza pneumonia. Immune and metabolic dysfunctions associated with the increased susceptibility to influenza infection are linked to obesity-associated low-grade inflammation, compromised immune and endocrine systems, and to high cardiovascular risk. These preexisting conditions may favor virological persistence, amplify immunopathological responses and worsen hemodynamic instability in severe COVID-19 as well. In this review we highlight the main factors and the current state of the art on obesity as risk factor for influenza and COVID-19 hospitalization, severe respiratory manifestations, extrapulmonary complications and even death. Finally, immunoregulatory mechanisms of severe influenza pneumonia in individuals with obesity are addressed as likely factors involved in COVID-19 pathophysiology.

Highlights

  • In December 2019, several cases of acute pneumonia of unknown etiology emerged in Wuhan, China

  • People with obesity are known to present changes at different innate and adaptive immune responses due to chronic low-grade inflammation (Karczewski et al, 2018). These preexisting responses may contribute to increased morbidity and mortality in severe respiratory diseases, since overwhelming cytokine production – known as cytokine storm – is a key pathological phenomenon in severe influenza pneumonia and COVID-19 (Gu et al, 2019; Coperchini et al, 2020; Ye et al, 2020)

  • The hypertrophy of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) are both positively correlated to metabolic risk factors, VAT expansion is closely associated with adverse metabolic complications (Fox et al, 2007)

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Summary

INTRODUCTION

In December 2019, several cases of acute pneumonia of unknown etiology emerged in Wuhan, China. Epidemiological evidences have shown obese COVID-19 patients at increased risk to require hospitalization, ICU admission and to evolve to death (Popkin et al, 2020) This increased susceptibility is positively correlated to the body mass index (BMI) with increasing risk of severity in overweight individuals, stage I obesity and stage II obesity. People with obesity are known to present changes at different innate and adaptive immune responses due to chronic low-grade inflammation (Karczewski et al, 2018) These preexisting responses may contribute to increased morbidity and mortality in severe respiratory diseases, since overwhelming cytokine production – known as cytokine storm – is a key pathological phenomenon in severe influenza pneumonia and COVID-19 (Gu et al, 2019; Coperchini et al, 2020; Ye et al, 2020).

IMMUNE RESPONSE IN OBESITY
The Dysfunctional Adipose Tissue in Obesity
Inflammatory Infiltrate in Adipose Tissue
Intestinal Hyperpermeability and Metabolic Endotoxemia
Is Adipose Tissue a Target for Viruses?
Findings
CONCLUSION
Full Text
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