Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
infection is an extremely contagious disease whereby the virus damages the host's respiratory tract via entering through the ACE2 receptor. Cardiovascular disorder is being recognized in the majority of
COVID-19 patients; yet, the relationship between SARS-CoV-2 and
heart failure has not been established. In the present study,
SARS-CoV-2 infection was induced in the monkey model. Thereafter, heart tissue samples were collected, and pathological changes were analyzed in the left ventricular tissue by
hematoxylin and
eosin, trichrome, and immunohistochemical staining specific to T lymphocytes and macrophages. The findings revealed that
SARS-CoV-2 infection induces several pathological changes in the heart, which cause cardiomyocyte disarray, mononuclear infiltrates of inflammatory cells, and
hypertrophy. Furthermore,
collagen-specific staining showed the development of cardiac
fibrosis in the interstitial and perivascular regions in the hearts of infected primates. Moreover, the myocardial tissue samples displayed multiple foci of inflammatory cells positive for T lymphocytes and macrophages within the myocardium. These findings suggest the progression of the disease, which can lead to the development of severe complications, including
heart failure. Additionally, SARS-CoV-2
antigen staining detected the presence of virus particles in the myocardium. Thus, we found that
SARS-CoV-2 infection is characterized by an exaggerated inflammatory immune response in the heart, which possibly contributes to myocardial remodeling and subsequent
fibrosis.