Aggravated pneumonia and diabetes in SARS-CoV-2 infected diabetic mice

Multiple clinical and epidemiological studies have shown an interconnection between coronavirus disease 2019 (COVID-19) and diabetes, but experimental evidence is still lacking. Understanding the interplay between them is important because of the global health burden of COVID-19 and diabetes. We found that C57BL/6J mice were susceptible to the alpha strain of SARS-CoV-2. Moreover, diabetic C57BL/6J mice with leptin receptor gene deficiency (db/db mice) showed a higher viral load in the throat and lung and slower virus clearance in the throat after infection than C57BL/6J mice. Histological and multifactor analysis revealed more advanced pulmonary injury and serum inflammation in SARS-CoV-2 infected diabetic mice. Moreover, SARS-CoV-2 infected diabetic mice exhibited more severe insulin resistance and islet cell loss than uninfected diabetic mice. By RNA sequencing analysis, we found that diabetes may reduce the collagen level, suppress the immune response and aggravate inflammation in the lung after infection, which may account for the greater susceptibility of diabetic mice and their more severe lung damage after infection. In summary, we successfully established a SARS-CoV-2 infected diabetic mice model and demonstrated that diabetes and COVID-19 were risk factors for one another.

Automated summary

Multiple studies have shown a connection between COVID-19 and diabetes, but experimental evidence is lacking. In this study, diabetic mice were found to have a higher viral load and slower virus clearance after SARS-CoV-2 infection compared to non-diabetic mice. Histological analysis revealed more severe lung damage and inflammation in diabetic mice. RNA sequencing analysis suggested that diabetes may suppress immune response and aggravate inflammation in the lung after infection. This study established a model to demonstrate that diabetes and COVID-19 are risk factors for each other.