Pathogenic parental rabies virus and apathogenic variant virus were shown to differ in their ability to infect neurons in vivo and neuroblastoma cells in vitro. After intracerebral inoculation, the distribution of infected neurons in the brain was similar for both viruses, but the rate of spread throughout the brain, the number of infected neurons, and the degree of cellular necrosis were much lower in the case of apathogenic virus. After adsorption to mouse neuroblastoma cells, apathogenic virus was less rapidly internalized than pathogenic virus, and cell-to-cell spread of apathogenic variant virus was completely prevented by the addition of rabies virus-neutralizing antibody, whereas the spread of pathogenic virus was not affected.

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Infant cats were inoculated intracranially with rabies or feline leukemia viruses in an experimental study of wasting syndrome. The daily pre- and postinoculation body weights were recorded until kittens were moribund. Affected animals in both groups manifested growth failure or wasting syndrome. Immunodepression, manifested by a conspicuous depletion of thymic cortex, the thymus dependent areas of the spleen, and growth hormone producing-alpha adenopituicytes was significantly (p less than 0.01) related to the wasting status of the animals. The ability of pituitary glands from these animals to produce growth hormone was studied by in situ immunoperoxidase staining and showed a significant (p less than 0.01) difference between healthy and wasted animals. Rabies and feline leukemia viruses were each found responsible for the low immunoreactivity of growth hormone producing alpha adenopituicytes. Because the hypothalamus and the hypophysis were both found infected, it was concluded that regardless of the triggering agent in primary wasting, the hypothalamic-hypophyseal-thymic axis was always involved through a decrease in growth hormone production.