Abstract
Murine hepatitis virus strain 3 (MHV-3) produces a strain dependent spectrum of liver disease. Mice of the A strain are fully resistant whereas Balb/cJ mice die of fulminant hepatic failure (1) . The susceptibility of inbred mice to MHV-3, is dependent on host factors which are under strict genetic control. Differences in viral replication both invivo and in-vitro do not appear to account for strain-dependent differences in resistance to MHV-3 and it has been suggested that variation in susceptibility/resistance of inbred mice reflects defects in the host–s immune response (2). Experimental ablation of the immune cell populations by X irradiation (3) , antilymphocyte serum (4) , or infection with frog virus-3 (5) renders resistant A/J mice susceptible. Furthermore, reconstitution of susceptible neonatal A/J mice with adult immune cells requires both T lymphocytes and an adherent cell population (6) . More recently, it has been demonstrated that clearance of virus from the central nervous system is dependent upon the presence of both CD4+ and CD8+ cells that recognize viral antigens in the context of H-2D gene products (7).
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© 1990 Plenum Press, New York
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Sinclair, S., Abecassis, M., Wong, P.Y., Romaschin, A., Fung, L.S., Levy, G. (1990). Mechanism of Protective Effect of Prostaglandin E in Murine Hepatitis Virus Strain 3 Infection: Effects on Macrophage Production of Tumour Necrosis Factor, Procoagulant Activity and Leukotriene B4. In: Cavanagh, D., Brown, T.D.K. (eds) Coronaviruses and their Diseases. Advances in Experimental Medicine and Biology, vol 276. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5823-7_74
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DOI: https://doi.org/10.1007/978-1-4684-5823-7_74
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