Inbred (C57BL; C3H/Bi), hybrid (C57BL x C3H/Bi), and outbred (TO) mice thymectomized within 24 hours of birth develop wasting symptoms and die prematurely and a proportion of these animals have pathological changes in the liver. The incidence of the liver lesions varies according to the strain of mice used and the lesions tend to occur in animals dying comparatively late.

These lesions were shown, by passage of tissue suspensions and of cell-free liver extracts, to be due to a hepatotrophic virus probably mouse hepatitis virus-1 (MHV-1). The part played by the hepatotrophic virus in the premature death of thymectomized mice is discussed but, although neonatal thymectomy apparently alters a normally stable host-virus relationship, it is not thought that the virus is primarily responsible for the death of its host. The role of this virus in the production of the physical wasting is also considered to be problematic.

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