Myocarditis in newborn wild-type BALB/c mice infected with the murine gamma herpesvirus MHV-68

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• 作者：Martin Hä ; usler ; Bernd Sellhaus ; Simone Scheithauer ; Bä ; rbel Gaida ; Sabrina Kuropka ; Katharina Siepmann ; Anna Panek ; Wibke Berg ; Andreas Teubner ; Klaus Ritter ; Michael Kleines
• 关键词：Murine gammaherpesvirus 68 ; MHV-68 ; Epstein– ; Barr virus ; Myocarditis ; Animal model ; Mouse
• 刊名：Cardiovascular Research
• 出版年：2007
• 期刊代码：48_00086363
• 类别：med
• 出版时间：1 November 2007
• 卷：76
• 期：2
• 页码：323-330
• 文件大小：940 K

摘要

Animal models of human Epstein–Barr virus (EBV) infection include EBV infection of primates and infection of mice with MHV-68, a further gamma herpesvirus (γ-HV). We aimed at extending the MHV-68 model to study γ-HV-related cardiac disease.

Methods

Newborn wild-type BALB/c- (n = 107), wild-type C57BL/6- (n = 17) and immunodeficient B6-(Rag1)™ mice (n = 18) were infected by nasal inoculation and evaluated for histopathological changes as well as tissue viral loads.

Results

From day 5 on BALB/c mice showed myocardial viral replication. Whereas focal inflammation occurred simultaneously, necrosis was first observed 9 days post-infection. The maximum rates of necrosis (40%) and of focal inflammation (33%) were found after 10 to 12 and 33 to 35 days, respectively. Some animals developed persistent viral activity and inflammation throughout the observation period of three months. Inflammation was mainly related to T cell infiltrates. Although C57BL/6 mice also showed myocardial inflammation, necrosis was not found suggesting differences in the susceptibility to the virus in distinct mouse strains. In immunodeficient animals higher myocardial viral loads were observed compared to wild-type mice but no cardiac lesions, which suggests that the antiviral immune response contributed to the lesions.

Conclusions

The model system presented here is the first to allow detailed studies on cardiac disease caused by γ-HV infections and may facilitate the development of more specific treatment options for human cardiac EBV infection.