Viral Infection and Connexin Dysfunction in the Heart.

Purpose of review: Gap junctions, comprising connexin proteins, enable the direct intercellular electrical coupling of cardiomyocytes, and disruption of this process is arrhythmogenic. In addition, gap junctions effect metabolic coupling and of relevance to this review, propagate host antiviral immune responses. Accordingly, connexins have emerged as viral targets during infection. This review summarizes current knowledge regarding contributions of inflammation vs virally encoded factors in driving alterations to cardiac gap junction function.

Recent findings: In addition to host immune-mediated effects on cardiac electrophysiology and gap junctions in myocarditis, there is now increasing appreciation for virally encoded factors targeting connexin function in acute/active infection. We now know diverse viral species have independently evolved to directly target connexin function during infection. Understanding both the direct and indirect effects of viral infection on cardiac gap junctions is critical to inform treatment strategies and development of novel therapeutics for acute infection as a distinct disease process from chronic myocarditis.