柯萨奇病毒和腺病毒受体的组织特异性缺失可保护小鼠免受病毒诱导的胰腺炎和心肌炎。
Tissue-specific deletion of the coxsackievirus and adenovirus receptor protects mice from virus-induced pancreatitis and myocarditis.
作者信息
Kallewaard Nicole L, Zhang Lili, Chen Jin-Wen, Guttenberg Marta, Sanchez Melissa D, Bergelson Jeffrey M
机构信息
Division of Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
出版信息
Cell Host Microbe. 2009 Jul 23;6(1):91-8. doi: 10.1016/j.chom.2009.05.018.
Abstract
In cultured cells, infection by group B coxsackievirus (CVB) is mediated by the coxsackievirus and adenovirus receptor (CAR), but the importance of this molecule in CVB-induced disease has not been determined. We generated mice with tissue-specific ablation of CAR within each of two major CVB target organs, the pancreas and heart. In the pancreas, deletion of CAR resulted in a significant reduction in both virus titers and virus-induced tissue damage. Similarly, cardiomyocyte-specific CAR deletion resulted in a marked reduction in virus titer, infection-associated cytokine production, and histopathology within the heart. Consistent with the in vivo phenotype, CAR-deficient cardiomyocytes resisted infection in vitro. These results demonstrate a critical function for CAR in the pathogenesis of CVB infection in vivo and in virus tropism for the heart and pancreas.
摘要
在培养细胞中，B组柯萨奇病毒（CVB）的感染由柯萨奇病毒和腺病毒受体（CAR）介导，但该分子在CVB诱导疾病中的重要性尚未确定。我们构建了在两个主要CVB靶器官（胰腺和心脏）中每个器官内CAR组织特异性缺失的小鼠。在胰腺中，CAR的缺失导致病毒滴度和病毒诱导的组织损伤均显著降低。同样，心肌细胞特异性CAR缺失导致心脏内病毒滴度、感染相关细胞因子产生和组织病理学显著降低。与体内表型一致，CAR缺陷的心肌细胞在体外抵抗感染。这些结果证明了CAR在体内CVB感染发病机制以及心脏和胰腺的病毒嗜性中起关键作用。
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