A recent review in eLife synthesises data from multiple studies to propose a synergistic interaction between SARS-CoV-2 infection and obesity and/or diabetes leading to impaired endothelial function and gut barrier function. This impairment results in microbial translocation into the systemic circulation and the ensuing cytokine storm. Adipocytes richly express ACE2 and are hence an easy target for SARS-CoV-2 infection and the establishment of a viral reservoir. ACE2 may also be shed from adipose tissue into the systemic circulation and deposited in the lungs and thus “modifying pulmonary susceptibility to SAR-CoV-2 infection”. Paradoxically, such an acute viral infection causes a reduction in ACE2 expression in other organs and tissues leading to ACE2 deficient expression elsewhere. This causes a disturbance of the ACE2:renin-angiotensin system (RAS). This can result in increased plasma levels of angiotensin II (Ang II), triggering vasoconstrictive responses. Ang II levels have shown correlations with the severity of lung injury in patients with severe COVID-19 and these disturbances are exacerbated in patients with obesity and diabetes. This injury can result in lung dysbiosis and bacteria and/or their products in the lungs promotes an additional lung injury resulting in “synergistic interaction between viral and bacterial pathogens”.
Obesity and diabetes as comorbidities for COVID-19: Underlying mechanisms and the role of viral–bacterial interactions.