Viral
myocarditis (VM) is an inflammatory disease of the myocardium associated with
heart failure, which is caused by common
viral infections. A majority of the
infections are initiated by coxsackievirus B3 (CVB3).
MicroRNAs (
miRNAs) have a major role in various biological processes, including gene expression, cell growth, proliferation, and apoptosis, as well as
viral infection and
antiviral immune responses. Although,
miRNAs have been found to regulate
viral infections, their role in CVB3
infection remains poorly understood. In the previous study,
miRNA microarray results showed that miR-324-3p expression levels were significantly increased when cells and mice were infected with CVB3. It was also found that miR-324-3p downregulated TRIM27 and decreased CVB3 replication in vitro and in vivo. In vitro, analysis of downstream signaling of TRIM27 revealed that, miR-324-3p inhibited CVB3
infection, and reduced cytopathic effect and viral plaque formation by reducing the expression of TRIM27. In vivo, miR-324-3p decreased the expression of TRIM27, reduced cardiac viral replication and load, thereby strongly attenuating cardiac injury and
inflammation. Taken together, this study suggests that miR-324-3p targets TRIM27 to inhibit CVB3 replication and viral load, thereby reducing the cardiac injury associated with VM.