Preferred Label : Viral Myocarditis Pathway;
NCIt related terms : Viral myocarditis;
Alternative definition : KEGG: Myocarditis is a cardiac disease associated with inflammation and injury of
the myocardium. It results from various etiologies, both noninfectious and infectious,
but coxsackievirus B3 (CVB3) is still considered the dominant etiological agent. Myocarditis
may be caused by direct cytopathic effects of virus, a pathologic immune response
to persistent virus, or autoimmunity triggered by the viral infection. The virus enters
the myocyte through internalization of the coxsackie-adenoviral receptor (CAR) and
its coreceptor, decay-accelerating factor (DAF). Viral proteases cleave various proteins
in the host cell. One example is viral protease 2A, which cleaves eukaryote initiation
factor 4G (eIF4G) and the dystrophin protein, resulting in a complete shutdown of
cap-dependent RNA translation and cytoskeletal destruction in infected cardiomyocytes,
respectively. CVB3 also cleaves the member of the Bcl-2 family Bid, leading to apoptosis.
CVB3 infection also induces the cleavage of cyclin D protein through a proteasome-dependent
pathway, leading to the host cell-growth arrest. Viral infection and necrosis of myocytes
may lead to the release of intracellular antigens, resulting in activation of self-reactive
T cells. CVB infection is a significant cause of dilated cardiomyopathy (DCM) as well
as myocarditis. Epidemiologically, myocarditis underlies a significant portion of
patients with DCM.;
KEGG ID : hsa05416;
Origin ID : C91441;
UMLS CUI : C2984254;
Automatic exact mappings (from CISMeF team)
Semantic type(s)
has_gene_product_element
pathway_has_gene_element