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Citation: Tingjun Liu, Jing Tong, Chen Shao, Junyan Qu, Hua Wang, Yi Shi, Yajing Lin, Yun Liu, Shihe Shao, Hongxing Shen. MicroRNA-324-3p Plays A Protective Role Against Coxsackievirus B3-Induced Viral Myocarditis [J].VIROLOGICA SINICA, 2021, 36(6) : 1585-1599.  http://dx.doi.org/10.1007/s12250-021-00441-4

MicroRNA-324-3p Plays A Protective Role Against Coxsackievirus B3-Induced Viral Myocarditis

  • Corresponding author: Shihe Shao, shaoshihe2006@163.com, ORCID: 0000-0001-9883-772X
    Hongxing Shen, hxshen@ujs.edu.cn, ORCID: 0000-0001-7311-5464
  • Received Date: 12 January 2021
    Accepted Date: 28 June 2021
    Published Date: 11 October 2021
    Available online: 01 December 2021
  • 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.


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    MicroRNA-324-3p Plays A Protective Role Against Coxsackievirus B3-Induced Viral Myocarditis

      Corresponding author: Shihe Shao, shaoshihe2006@163.com
      Corresponding author: Hongxing Shen, hxshen@ujs.edu.cn
    • 1. School of Medicine College, Jiangsu University, Zhenjiang, 212013, China
    • 2. Xuzhou Municipal Center for Disease Control and Prevention, Xuzhou, 221006, China
    • 3. Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212000, China
    • 4. Center of Infectious Disease, West China Hospital Sichuan University, Chengdu, 610041, China

    Abstract: 

    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.