Mouse hepatitis virus infection utilizes more than one receptor and requires an additional cellular factor.

Abstract

Mouse hepatitis virus (MHV) causes hepatitis, encephalomyelitis, respiratory and gastrointestinal ailments. Our laboratory has been particularly interested in the mechanism of neuropathogenesis of MHV. Different MHV strains have different capacities to cause central nervous system (CNS) infection. Among the neurotropic strains, there is also a large degree of variation in their ability to cause encephalitis or demyelination. Various virus variants have been obtained from the neurotropic MHV strains which show altered neuropathogenicity; for example, many of the variants which escape neutralization by the spike (S) protein-specific monoclonal antibodies differ from the parental viruses in not causing encephalitis, but still retain the ability to cause demyelination (Fleming et al., 1986; Dalziel et al., 1986). These variants have either point mutations or deletions in the viral spike protein (Gallagher et al., 1990; Wang et al., 1992). Since the S protein presumably interacts with the viral receptor on the surface of target cells, it is reasonable to assume that the difference in the viral neurotropism is caused by the variations in their ability to interact with the receptors. Therefore, it is conceivable that the MHV receptors in different cell types, e.g. neurons, astrocytes or oligodendrocytes, in CNS might be different.KeywordsViral ReceptorMouse Hepatitis VirusHoward Hughes Medical InstituteMouse Hepatitis Virus StrainMouse Hepatitis Virus InfectionThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.