Zika Virus Infection Downregulates Connexin 43, Disrupts the Cardiomyocyte Gap Junctions and Induces Heart Diseases in A129 Mice
Shuxuan Li, Najealicka Armstrong, Huan Zhao, Ruth Cruz‐Cosme, Hong-Wei Yang, Chunlian Zhong, Wenkun Fu, Wei Wang, Decheng Yang, Ningshao Xia, Tong Cheng, Qiyi Tang
Abstract
Zika virus (ZIKV) is a teratogen causing devastating sequelae to the newborns who suffer a congenital ZIKV infection while it brings about only mild symptoms to the health-competent older children or adults. Mouse models have played an important role in mechanistic and pathogenic studies of ZIKV. In this study, we employed 3 to 4 week-old A129 mice for ZIKV infection. RT-qPCR assays discovered that ZIKV replicated in multiple organs, including the heart. As a result of ZIKV infection, the A129 mice experienced weight loss, health score worsening, paralysis, and deaths. We revealed that the ZIKV infection caused abnormal electrocardiogram presentations, increased cardiac muscle enzymes, downregulated Cx43, and destroyed the gap junction and the intercalated disc between the cardiomyocytes, implicating that ZIKV may cause an acute myocardial injury in A129 mice. Therefore, our data imply that ZIKV infection may jeopardize the immunocompromised population with a severe clinical consequence, such as heart defect.