Abstract
Murine hepatitis virus type 3 (MHV-3) produces a strain dependent pattern of disease in inbred strains of mice. Balb/cJ mice develop fulminant hepatitis following MHV-3 infection.1. Direct viral cytopathic effects do not account for the full spectrum of the disease and it appears that host immune factors are important in the pathogenesis of the disease. We have previously demonstrated that the induction of a specific macrophage protease (procoagulant activity (PCA)) correlates directly with susceptibility to disease and that it is responsible for disturbances in the microcirculation characterized by microthrombi, vasculitis, thrombosis and cellular necrosis.2. Little attention has been devoted to the effects of prostaglandins on viral infections. These studies were undertaken to examine the effect of 16, 16 dimethyl prostaglandin E2 on an experimental animal model of viral hepatitis.
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Levy, G., Leibowitz, J. L., Edgington, T. S. Journal of Experimental Medicine 154: 1150: 1981.
Macphee, P.J., Dindzans, V.J., Fung, L.S., Levy, G.A. Hepatology 5: 649: 1985.
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© 1987 Plenum Press, New York
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Abecassis, M. et al. (1987). Prostaglandin E2 (PGE2) Alters the Pathogenesis of MHV-3 Infection in Susceptible Balb/cJ Mice. In: Lai, M.M.C., Stohlman, S.A. (eds) Coronaviruses. Advances in Experimental Medicine and Biology, vol 218. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1280-2_58
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DOI: https://doi.org/10.1007/978-1-4684-1280-2_58
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