柯萨奇病毒B3诱导远交系NMRI小鼠发生慢性心肌炎。

Coxsackievirus B3-induced chronic myocarditis in outbred NMRI mice.

作者信息

Merkle I, Tonew M, Glück B, Schmidtke M, Egerer R, Stelzner A

机构信息

Institute of Virology, Clinical Center of the Friedrich Schiller University, Jena, Germany.

出版信息

J Hum Virol. 1999 Nov-Dec;2(6):369-79.

PMID:10774554

Abstract

OBJECTIVES

The pathogenesis of coxsackievirus B3 (CVB3)-induced myocarditis was investigated in adult Han:NMRI mice. The outbred model, in comparison with inbred models, represents better the natural variable susceptibility of the human population.

STUDY DESIGN/METHODS: We analyzed the replicating virus titer, the antibody response in the acute and chronic phase of disease, the histology of myocardial injury, and the persistence of viral RNA.

RESULTS

NMRI mice infected with 5000 plaque-forming units (PFU) of the CVB3 variant "P"D, a lytic variant to human fibroblast lines, showed a peak of virus replication at day 14 and developed a severe acute myocarditis. The chronic myocarditis was characterized by progressive fibrosis, small foci of infiltrates, persistent viral RNA in the heart, and detectable anti-CVB3 IgG production and neutralizing antibody response up to day 98 postinfection.

CONCLUSIONS

CVB3"P"D is able to induce chronic myocarditis in NMRI mice. This model provides a method for examining and proving the mechanisms of myocardial pathogenesis and of developing therapeutic strategies.

摘要

目的

在成年Han:NMRI小鼠中研究柯萨奇病毒B3（CVB3）诱导的心肌炎的发病机制。与近交系模型相比，远交系模型能更好地代表人类群体自然的易感性差异。

研究设计/方法：我们分析了复制病毒滴度、疾病急性期和慢性期的抗体反应、心肌损伤的组织学以及病毒RNA的持续性。

结果

感染5000个噬斑形成单位（PFU）的CVB3变异株“P”D（一种对人成纤维细胞系具有裂解性的变异株）的NMRI小鼠，在第14天出现病毒复制高峰，并发展为严重的急性心肌炎。慢性心肌炎的特征为进行性纤维化、小灶性浸润、心脏中持续存在病毒RNA，以及在感染后第98天可检测到抗CVB3 IgG产生和中和抗体反应。