Genetic resistance to mouse hepatitis virus correlates with absence of virus-binding activity on target tissues.
The molecular mechanism of genetic resistance of inbred mouse strains to mouse hepatitis virus, a murine coronavirus, was studied by comparing virus binding to plasma membranes of intestinal epithelium or liver from susceptible BALB/c and resistant SJL/J mice with a new solid-phase assay for virus-binding activity. Virus bound to isolated membranes from susceptible mice, but not to membranes from resistant mice. F1 progeny of SJL/J X BALB/c mice had an intermediate level of virus-binding activity on their enterocyte and hepatocyte membranes. This correlated well with previous studies showing that susceptibility to mouse hepatitis virus strain A59 is controlled by a single autosomal dominant gene (M. S. Smith, R. E. Click, and P. G. W. Plagemann, J. Immunol. 133:428-432). Because virus binding was not prevented by treating membranes with sodium dodecyl sulfate, the virus-binding molecule could be identified by a virus overlay protein blot assay. Virus bound to a single broad band of Mr 100,000 to 110,000 in membranes from hepatocytes or enterocytes of susceptible BALB/c and semisusceptible C3H mice, but no virus-binding band was detected in comparable preparations of resistant SJL/J mouse membranes. Therefore, SJL/J mice may be resistant to mouse hepatitis virus A59 infection because they lack a specific virus receptor which is present on the plasma membranes of target cells from genetically susceptible BALB/c and semisusceptible C3H mice.
D000818:Animals; D000914:Antibodies, Viral; D000956:Antigens, Viral / Q000032:analysis; D002462:Cell Membrane / Q000382:microbiology; D006524:Hepatitis, Viral, Animal / Q000276:immunology*; D007113:Immunity, Innate; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D006517:Murine hepatitis virus / Q000276:immunology*; D011991:Receptors, Virus / Q000032:analysis
D000914:Antibodies, Viral; D000956:Antigens, Viral; D011991:Receptors, Virus