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

doi:10.1016/j.cardiores.2007.06.025

Cardiovascular Research 2007 76(2):323-330; doi:10.1016/j.cardiores.2007.06.025

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

Martin Häusler^a^,*, Bernd Sellhaus^b, Simone Scheithauer^c, Bärbel Gaida^a^,b, Sabrina Kuropka^c, Katharina Siepmann^a^,b, Anna Panek^b, Wibke Berg^a^,c, Andreas Teubner^d, Klaus Ritter^c and Michael Kleines^c

^aDepartment of Pediatrics, University Hospital, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany
^bDepartment of Neuropathology, University Hospital, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany
^cDivision of Virology/Institute of Medical Microbiology, University Hospital, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany
^dInstitute of Laboratory Animal Science, University Hospital, RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany

*Corresponding author. Tel.: +49 241 800; fax: +49 241 8082484. Haeusler{at}rwth-aachen.de

Objectives Animal models of human Epstein–Barr virus (EBV)infection include EBV infection of primates and infection ofmice with MHV-68, a further gamma herpesvirus ( ${delta}$ -HV). We aimedat extending the MHV-68 model to study ${delta}$ -HV-related cardiac disease.

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

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

Conclusions The model system presented here is the first toallow detailed studies on cardiac disease caused by ${delta}$ -HV infectionsand may facilitate the development of more specific treatmentoptions for human cardiac EBV infection.

KEYWORDS Murine gammaherpesvirus 68; MHV-68; Epstein–Barr virus; Myocarditis; Animal model; Mouse

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