COVID-19 works with the body's microbiota to increase diseas
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The combined effects of the body's microbiota working together with COVID-19 in the lungs could explain the severity of the disease in people with obesity and diabetes, according to a new article published today in eLife.

The review offers important mechanistic insights into why people with obesity and diabetes seem to be at increased risk of developing severe acute respiratory syndrome (SARS) after infection with the COVID-19 virus, and more often require hospitalisation and ventilation.

Obesity and diabetes are established comorbidities for COVID-19. Adipose tissue demonstrates high expression of ACE2 which SARS- CoV-2 exploits to enter host cells. This makes adipose tissue a reservoir for SARS-CoV-2 viruses and thus increases the integral viral load. Acute viral infection results in ACE2 downregulation.

This relative deficiency can lead to disturbances in other systems controlled by ACE2, including the renin-angiotensin system. This will be further increased in the case of pre-conditions with already compromised functioning of these systems, such as in patients with obesity and diabetes. Here, we propose that interactions of virally-induced ACE2 deficiency with obesity and/or diabetes leads to a synergistic further impairment of endothelial and gut barrier function.

The appearance of bacteria and/or their products in the lungs of obese and diabetic patients promotes interactions between viral and bacterial pathogens, resulting in a more severe lung injury in COVID-19.