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Among the many models of experimental viral infections, the mouse hepatitis virus (MHV) model offers a number of advantages for investigation of the host-virus relationship: 1. MHV infection is a naturally occurring infection in the mouse (Rowe et al. 1963); Broderson et al. 1976; Ishida et al. 1978) and thus is not an artificial model. 2. In the case of mouse hepatitis virus type 3 (MHV-3), the natural resistance is observed to various degrees according to the mouse strain considered (Virelizier and Allison 1976), with either full susceptibility, full resistance, or semiresistance being present This provides the opportunity to make correlations with parameters of the immune response in a more precise manner than in other models where only two situations (susceptibility and resistance) are observed. 3. The mouse strains showing variable degrees of susceptibility to MHV-3 (namely, A/J, C3H/He, and C57/BL-6) are well-known inbred strains whose biologic parameters have been thoroughly investigated. 4. MHV infections have been among the first models in which the role of macrophages in host defense have been investigated after the pioneering studies of F. Bang and his colleagues (Bang and Warwick 1960; Shif and Bang 1970). 5. MHV-3 induces a very easily recognizable cytopathic effect in mouse macrophage cultures by fusing infected macrophages into multinucleated giant cells (Malucci 1965). The appearance of this cytopathic effect closely parallels the intensity of viral replication and thus provides a useful tool for in vitro studies in macrophages from different strains of mice (Virelizier and Allison 1976). 6. MHV-3 infection is so far the only Coronavirus model in which the protective role of interferon in vivo has been demonstrated (Virelizier and Gresser 1978). 7. Finally, the modification of immune responsiveness during acute or persistent infections has been investigated (Virelizier et al. 1976). |
