Tissue-Specific Deletion of the Coxsackievirus and Adenovirus Receptor Protects Mice from Virus-induced Pancreatitis and Myocarditis

被引：53

作者：

Kallewaard, Nicole L. ^{[1
]}

Zhang, Lili ^{[1
]}

Chen, Jin-Wen ^{[1
]}

Guttenberg, Marta ^{[2
,4
]}

Sanchez, Melissa D. ^{[5
]}

Bergelson, Jeffrey M. ^{[1
,3
]}

机构：

[1] Childrens Hosp Philadelphia, Div Infect Dis, Philadelphia, PA 19104 USA

[2] Childrens Hosp Philadelphia, Dept Pathol, Philadelphia, PA 19104 USA

[3] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA

[4] Univ Penn, Sch Med, Dept Pathol, Philadelphia, PA 19104 USA

[5] Univ Penn, Sch Vet Med, Dept Toxicol & Pathol, Philadelphia, PA 19104 USA

来源：

CELL HOST & MICROBE | 2009年 / 6卷 / 01期

关键词：

VIRAL MYOCARDITIS; IN-VIVO; INFECTION; EXPRESSION; PATHOGENESIS; HEXON; CELLS; MODEL; CROSS; ENTRY;

D O I：

10.1016/j.chom.2009.05.018

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

引用

页码：91 / 98

页数：8

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