Estudo dos distúrbios cardíacos induzidos por betacoronavírus em modelo murino de obesidade

Abstract

Covid-19 caused a global impact on health, with millions of fatalities, most of whom already had some type of comorbidity. Scientific evidence has revealed that obese patients have a significantly increased risk of developing severe forms of Covid-19. Although COVID-19 is known as a severe acute respiratory syndrome (SARS), it presents with a wide range of symptoms that often include heart disease. Among the complications of the disease, the following stand out: viral myocarditis, indirect cardiac injury, stress cardiomyopathy, heart failure (HF) and arrhythmias. Furthermore, among the factors that can further aggravate cardiovascular damage induced by SARS-CoV-2 infection, obesity is of special interest, after all, it causes direct cardiac complications. Given this context, we raise the hypothesis that an infection analogous to SARS-CoV-2 (by MHV-A59), in a murine model of obesity, aggravates coronavirus-induced cardiac damage. To test this hypothesis, we subjected C57BL/6 mice to a standard or cafeteria diet (Caf) for 4 weeks. We then instilled saline or murine hepatitis virus strain A59 (MHV-A59) into the nostrils of mice and evaluated the hearts and other organs after 8 days of infection. Our main findings were that the short time on the Coffee diet was sufficient to promote increased adiposity, insulin resistance and cardiomyocyte hypertrophy. After pulmonary infection with MHV-A59, hearts from mice on a standard diet showed few signs of injury, but showed a greater response to ex vivo adrenergic stimulation. Hearts from infected Caf diet animals showed an increase in oxidative stress protectors, greater fibrosis, without changes in ex vivo cardiac function. We conclude that obesity and betacoronavirus infection cause deleterious cardiac effects both individually and together. The combined effects result in increased fibrosis and oxidative stress in the heart.