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KMID : 0921620130430030210
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Journal of Bacteriology and Virology
2013 Volume.43 No. 3 p.210 ~ p.216
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Cardiac-specific Coxsackievirus and Adenovirus Receptor (CAR) Deletion Inhibit Enterovirus Infection in Murine Heart
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Kim Jin-Hee
Seok Heon
Lim Byung-Kwan
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Abstract
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The structure of coxsackievirus and adenovirus receptor's CAR is similar to adhesion molecules. In the adult heart, the majority of CAR localizes at the intercalated disc. Germ line CAR deletion induces embryonic lethality at E11.5 with evidence of a cardiac abnormality. The CAR role as a viral receptor is well known; however, its precise function in the heart for enterovirus infection is not clear. To understand the role of CAR in the cardiac myocyte, we generated cardiac-specific CAR knockout mice using a CAR floxed allele and alpha-MHC-Mer CRE Mer mice. Western blot analysis and immunofluorescent stain of ventricles at 6 weeks after 2 weeks tamoxifen administration, CAR expression was significantly decreased in CARf/f MCM mice but not in CARf/f mice heart. Enterovirus was intraperitoneally infected into CARf/f MCM and CARf/f mice (n=10 each). CAR disruption was dramatically reduced virus infection and replication in the heart but not different in liver, spleen, and pancreas. Cardiac myocyte damage was significantly reduced in the CARf/f MCM mutant mice by evans blue dye stain. In addition, the CARf/f MCM mutant mice heart inflammation and fibrosis were decreased in H&E and trichrome stain compare to CARf/f control mice. CAR expression was required for normal ventricular function, but it is the cause of enterovirus infection. In the adult mice heart, CAR deletion was significantly reduced viral infection, proliferation, and myocarditis. These results suggested that CAR deletion could be useful therapeutic strategy to prevent viral myocarditis.
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KEYWORD
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Coxsackievirus and adenovirus receptor, Cardiomyocyte, Enterovirus, Inflammation, Myocaditis
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