Abstract
Myocarditis, or inflammation of the muscle layer in the heart wall, is caused by several factors including viral infection. Although the literature briefly alludes to a method of viral entry into cardiomyocytes, this work provides further detail into subsequent novel mechanisms leading to the development of myocarditis following infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The keywords "COVID-19”, “SARS-CoV-2”, “Myocarditis”, “viruses”, and “human” were used to run searches on OVID Medline, as well as Google Scholar. Resulting papers were subject to further analysis. SARS-CoV-2 binds to the angiotensin-converting enzyme 2 (ACE2) receptor which is found on type 2 pneumocytes and cardiomyocytes. Infection of cardiomyocytes can overregulate the immune response resulting in a cytokine storm: an uncontrolled increase of proinflammatory cytokines, as is commonly seen in respiratory infections. Cytokines can enter established biological pathways, creating positive feedback, which causes increased inflammation leading to myocarditis. SARS-CoV-2 viral envelope (E) proteins present an alternate association with myocarditis. Less severe myocarditis manifests common symptoms, and detecting it before it worsens may be difficult. Understanding the pathogenesis of myocarditis in COVID-19 could help find and implement preventative measures during future treatment.
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