Neutralizing and nonneutralizing monoclonal antibodies to the peplomer glycoprotein and nucleocapsid protein of a mouse hepatitis virus (MHV), MHV-NuU, protected mice against lethal MHV-2 challenge. Histopathologically, livers of mice receiving protective antibodies showed some focal necrotic lesions with remarkable cellular infitration instead of fulminant hepatitis caused by MHV-2. Mouse hepatitis virus (MHV) is a member of the coronavirus group producing both acute and chronic diseases in various species of animals (15, 17, 25). Most MHV strains have been shown to have the nucleocapsid protein (NP) and the minor (El) and major (E2) envelope glycoproteins (18, 19). El is probably of the viral matrix, whereas E2 forms the peplomers that have important roles in attachment to host cells (18, 19). We described previously the production of monoclonal antibodies (MAbs) to low-virulence MHV-NuU, an isolate from a wasted nude mouse (7), and their specificity for viral polypeptides (10). Those MAbs were shown to be crossreactive in vitro with other strains of MHV including the highly hepatitogenic strain MHV-2 (6, 11, 12). This paper describes protective effects of MAbs against E2 as well as NP of MHV-NuU in highly virulent MHV-2 infection in mice.
Mouse hepatitis virus (MHV)-specific T-lymphocyte clones were established from MHV-infected BALB/c mice. They expressed Thyl and Lyt2 antigens but lacked L3T4 and NK1 antigens. The clones killed MHV-infected but not uninfected or influenza virus-infected J774.1 cells. The specificity was further defined by a cold-target competition test.
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