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Coxsackievirus A2 Leads to Heart Injury in a Neonatal Mouse Model

Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou 450001, China
Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
School of Public Health, Xinxiang Medical University, Xinxiang 453003, China
Henan Key Laboratory of Molecular Medicine, Zhengzhou University, Zhengzhou 450001, China
Authors to whom correspondence should be addressed.
Academic Editors: Charu Kaushic and Amy Gillgrass
Received: 7 June 2021 / Revised: 30 July 2021 / Accepted: 2 August 2021 / Published: 11 August 2021
(This article belongs to the Special Issue In Vivo Mouse Models of Human Viral Infections)
Coxsackievirus A2 (CVA2) has emerged as an active pathogen that has been implicated in hand, foot, and mouth disease (HFMD) and herpangina outbreaks worldwide. It has been reported that severe cases with CVA2 infection develop into heart injury, which may be one of the causes of death. However, the mechanisms of CVA2-induced heart injury have not been well understood. In this study, we used a neonatal mouse model of CVA2 to investigate the possible mechanisms of heart injury. We detected CVA2 replication and apoptosis in heart tissues from infected mice. The activity of total aspartate transaminase (AST) and lactate dehydrogenase (LDH) was notably increased in heart tissues from infected mice. CVA2 infection also led to the disruption of cell-matrix interactions in heart tissues, including the increases of matrix metalloproteinase (MMP)3, MMP8, MMP9, connective tissue growth factor (CTGF) and tissue inhibitors of metalloproteinases (TIMP)4. Infiltrating leukocytes (CD45+ and CD11b+ cells) were observed in heart tissues of infected mice. Correspondingly, the expression levels of inflammatory cytokines in tissue lysates of hearts, including tumor necrosis factor alpha (TNF-α), interleukin-1beta (IL-1β), IL6 and monocyte chemoattractant protein-1 (MCP-1) were significantly elevated in CVA2 infected mice. Inflammatory signal pathways in heart tissues, including phosphatidylinositol 3-kinase (PI3K)-AKT, mitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-κB), were also activated after infection. In summary, CVA2 infection leads to heart injury in a neonatal mouse model, which might be related to viral replication, increased expression levels of MMP-related enzymes and excessive inflammatory responses. View Full-Text
Keywords: hand, foot and mouth disease; coxsackievirus A2; matrix metalloproteinase; heart injury hand, foot and mouth disease; coxsackievirus A2; matrix metalloproteinase; heart injury
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MDPI and ACS Style

Ji, W.; Zhu, P.; Liang, R.; Zhang, L.; Zhang, Y.; Wang, Y.; Zhang, W.; Tao, L.; Chen, S.; Yang, H.; Jin, Y.; Duan, G. Coxsackievirus A2 Leads to Heart Injury in a Neonatal Mouse Model. Viruses 2021, 13, 1588.

AMA Style

Ji W, Zhu P, Liang R, Zhang L, Zhang Y, Wang Y, Zhang W, Tao L, Chen S, Yang H, Jin Y, Duan G. Coxsackievirus A2 Leads to Heart Injury in a Neonatal Mouse Model. Viruses. 2021; 13(8):1588.

Chicago/Turabian Style

Ji, Wangquan, Peiyu Zhu, Ruonan Liang, Liang Zhang, Yu Zhang, Yuexia Wang, Weiguo Zhang, Ling Tao, Shuaiyin Chen, Haiyan Yang, Yuefei Jin, and Guangcai Duan. 2021. "Coxsackievirus A2 Leads to Heart Injury in a Neonatal Mouse Model" Viruses 13, no. 8: 1588.

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