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两种柯萨奇病毒B3毒株的比较分析:病毒-受体相互作用对发病机制的潜在影响

Comparative analysis of two coxsackievirus B3 strains: putative influence of virus-receptor interactions on pathogenesis.

作者信息

Selinka H-C, Wolde A, Pasch A, Klingel K, Schnorr J-J, Küpper J-H, Lindberg A M, Kandolf R

机构信息

Department of Molecular Pathology, University Hospital Tübingen, Tübingen, Germany.

出版信息

J Med Virol. 2002 Jun;67(2):224-33. doi: 10.1002/jmv.2211.

DOI:10.1002/jmv.2211
PMID:11992583
Abstract

Strain-specific differences in the interaction of coxsackievirus B3 (CVB3) with the coxsackievirus-adenovirus receptor (CAR) and the decay-accelerating factor (DAF) co-receptor proteins were investigated using a non-haemagglutinating (CVB3) and a haemagglutinating (CVB3-HA) strain of CVB3. A panel of receptor-transfected hamster CHO cells, expressing either CAR (CHOCAR cells), DAF (CHODAF cells), or both receptor proteins (CHODC cells) were used to study the interplay of CAR and DAF receptor molecules with regard to binding and infection with CVB3 and CVB3-HA. Despite clear differences in their binding phenotypes, both virus strains were found to primarily depend on the CAR receptor protein for initialization of productive infections. Cytopathic effects induced by CVB3-HA were influenced by co-expression of DAF receptor proteins. The cardiotropic potential of both virus strains was investigated in A.BY/SnJ mice. Despite comparable virus replication of both CVB3 strains in individual myocytes, the number of infected heart muscle cells was significantly lower in CVB3-HA infected mice. Infections of pancreata correlated with myocardial infections. Together these data suggest that even small differences in virus-receptor interactions, influencing virus binding and virus spread, may have an impact on the pathogenesis of CVB-induced diseases.

摘要

利用柯萨奇病毒B3(CVB3)的非血凝(CVB3)和血凝(CVB3-HA)毒株,研究了CVB3与柯萨奇病毒-腺病毒受体(CAR)和衰变加速因子(DAF)共受体蛋白相互作用中的毒株特异性差异。使用一组转染了受体的仓鼠CHO细胞,这些细胞分别表达CAR(CHOCAR细胞)、DAF(CHODAF细胞)或两种受体蛋白(CHODC细胞),以研究CAR和DAF受体分子在CVB3和CVB3-HA结合及感染方面的相互作用。尽管它们的结合表型存在明显差异,但发现两种病毒毒株主要依赖CAR受体蛋白来启动有效感染。DAF受体蛋白的共表达影响了CVB3-HA诱导的细胞病变效应。在A.BY/SnJ小鼠中研究了两种病毒毒株的嗜心性潜力。尽管两种CVB3毒株在单个心肌细胞中的病毒复制相当,但CVB3-HA感染小鼠中受感染的心肌细胞数量明显较少。胰腺感染与心肌感染相关。这些数据共同表明,即使病毒-受体相互作用中的微小差异,影响病毒结合和病毒传播,也可能对CVB诱导疾病的发病机制产生影响。

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