Abstract
In the attempt to develop a homogeneous neuronal model to study rabies pathogenesis in vivo and in vitro, the superior cervical ganglia (SCG) were chosen because of their unique features. In vivo infection of the SCG was attempted by inoculation of fixed rabies virus into the anterior eye chamber. However, viral by this route as well as intracerebrally failed to infect this neuronal organ in adult rats whereas the infection was poorly efficient in 24 hours newborn rats. Dissociated cell cultures from the rat embryo SCG were infected in vitro and examined for the presence of rabies specific antigen and release of virus particles in the supernatant. Despite the presence of rabies nucleoprotein in the cytoplasm and the presence of typical Negri bodies, neurons from the rat SCG produced few particles as observed by electron microscopy and no increase in virus yields could be detected by titration of viral infectivity during the infectious cycle. Our observations indicate that although rabies virus is neurotropic as shown in previous studies, all neuronal tissues are not equally susceptible to this viral infection. The resistance of the SCG to rabies virus infection in vivo does not seems to be a lack of accessibility of this organ to infection since other authors had shown that it could be infected by herpes virus. Both in vitro and in vivo experiments show that although neurons from the SCG are susceptible to rabies virus infection, infected cells do not produce rabies infectious virions efficiently.
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