Hritika Nandakumar

Molecular mechanisms of Coxsackievirus and Epstein-Barr virus-induced myocarditis

Started Oct. 13, 2023

Abstract or project description

Coxsackievirus and Epstein-Barr virus (EBV) are two distinct viruses that can cause myocarditis, which is the inflammation of the heart muscle. The molecular mechanisms underlying the development of myocarditis due to these viruses are complex and involve various interactions between the viruses and the host immune system. The virus gains entry into cardiac cells, often through specific receptors on the cell surface.Viral replication occurs within the cardiac myocytes, leading to the production of viral progeny. The host immune system recognizes the viral infection and mounts an immune response to eliminate the virus. Inflammatory cells, such as macrophages and T lymphocytes, infiltrate the myocardium in an attempt to clear the virus. The immune response triggers the release of various cytokines, such as interleukins (IL), tumor necrosis factor-alpha (TNF-α), and interferons. Excessive cytokine production can lead to a cytokine storm, causing widespread inflammation and tissue damage, including damage to the myocardium. Viral replication and the host immune response can induce apoptosis (programmed cell death) and necrosis of cardiac myocytes. Cell death contributes to the release of cellular contents, activating the immune system further and exacerbating inflammation. In some cases, the immune response can become dysregulated, leading to the generation of autoantibodies targeting the host's own cardiac proteins. Autoimmune reactions can perpetuate inflammation and contribute to the development of myocarditis.