Abstract
Myocarditis underlies 42% of sudden cardiac death in young adults, yet viral arrhythmogenic mechanisms remain elusive. Adenovirus is a leading cause but species-specificity has limited disease modeling in mice. Gap junctions, composed primarily of connexin43 (Cx43), enable electrical impulse propagation in the heart. Changes in Cx43 expression, localization, and/or function cause arrhythmias. Gap junctions propagate innate and adaptive antiviral responses, and our prior work has demonstrated that Cx43 expression and function are reduced during human adenoviral infection.
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