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J Gen Virol 74 (1993), 1381-1391; DOI 10.1099/0022-1317-74-7-1381
© 1993 Society for General Microbiology
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Dilated heart failure in transgenic mice expressing the Epstein—Barr virus nuclear antigen-leader protein

David S. Huen1, Andrew Fox2, Prem Kumar2 and Peter F. Searle1

1 Cancer Research Campaign Laboratories, Department of Cancer Studies
and2 Department of Physiology, University of Birmingham Medical School, Birmingham B15 2TJ, U.K.

The Epstein—Barr virus nuclear antigen-leader protein (EBNA-LP) is required for high efficiency B lymphocyte growth transformation by the virus. To test the potential contribution of EBNA-LP to tumorigenesis in vivo, we produced transgenic mice carrying an EBNA-LP cDNA construct, using the widely expressed metallothionein promoter. Expression of EBNA-LP was detected in liver, kidney, heart, lung and spleen. There were no apparent oncogenic consequences of EBNA-LP expression. Unexpectedly however, at ages ranging from about 4 months to over a year, transgenic mice developed symptoms of congestive heart failure, including left ventricular dilatation, right ventricular hypertrophy, left atrial thrombosis, pulmonary oedema and hydrothorax. Fibrillation was not apparent in the electrocardiograph; however a reduction in T-wave amplitude suggested that the development of an abnormality of ventricular repolarization may precede the manifestation of overt symptoms. The highly predictable development of dilated heart failure in these transgenic mice suggests they may be a useful model for the pathophysiological changes associated with human dilated cardiomyopathy.

Received 20 October 1992; accepted 15 February 1993.


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