From Influenza Virus to Novel Corona Virus (SARS-CoV-2)-The Contribution of Obesity

Abstract

From the beginning of 2020, the governments and the health systems around the world are tackling infections and fatalities caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) resulting in the coronavirus disease 2019 (COVID-19). This virus pandemic has turned more complicated as individuals with co-morbidities like diabetes, cardiovascular conditions and obesity are at a high risk of acquiring infection and suffering from a more severe course of disease. Prolonged viral infection and obesity are independently known to lower the immune response and a combination can thus result in a "cytokine storm" and a substantial weakening of the immune system. With the rise in obesity cases globally, the chances that obese individuals will acquire infection and need hospitalization are heightened. In this review, we discuss why obesity, a low-grade chronic inflammation, contributes toward the increased severity in COVID-19 patients. We suggest that increased inflammation, activation of renin-angiotensin-aldosterone system, elevated adipokines and higher ectopic fat may be the factors contributing to the disease severity, in particular deteriorating the cardiovascular and lung function, in obese individuals. We look at the many lessons learnt from the 2009 H1N1 influenza A pandemic and relate it to the very little but fast incoming information that is available from the SARS-CoV-2 infected individuals with overweight and obesity.

Keywords: COVID-19; SARS-CoV-2; adipocytes; adiposity; novel corona virus; obesity.

Figure 1

Excess adiposity provides an ideal setting to promote viral infection. We propose that obesity and its associated conditions elevate the cytokines, adipokines and RAAS and increase ectopic fat accumulation. When infection sets in, in this case with SARS-COV-2, through ACE2 receptor on the adipose tissue, the lungs, the heart and the blood vessels, the virus enters, mediates a cytokine storm and creates an imbalance in AngII/ACE-2 levels, elevates leptin levels and lowers anti-viral molecules like IFNs. Moreover, adipose tissue a might serve as a reservoir for viral persistence, which could be the possible source of continuous viral shedding and systemic inflammation. The combination of all the factors deteriorates lungs and the cardiovascular system, weakens the immune response, and promotes viral shedding. Yellow circle indicate adipocytes, red marks indicate inflammatory cells, upwards and downwards arrows indicates upregulation or downregulation of molecules and/ or effect.