Mouse Models

Mice are readily infected and have high titers ofvirus in brain. Disease can be induced by adaptation of virus through multiple passages in mice or infection of specific host strains during the neonatal period. As in rats, severe clinical disease is mediated by MHC class I restricted cytotoxic T cells. A model of subtle behavioral disease has been reported in mutant mice that lack functional CD8 cells (C57BL/10J mice) wherein maze performance was correlated with IP-10 expression independent of frank histopathology.

D. Tree Shrews

Little is known about BDV pathogenesis in phylogen-etically higher species such as nonhuman primates and the prosimian tree shrews (Tupaia glis). Intracerebral inoculation of tree shrews leads to persistent infections and a disorder characterized primarily by hyperactiv-ity and alterations in sociosexual behavior rather than motor dysfunction. Disturbances in breeding and social behavior were most profound in animals caged in mating pairs. Females rather than males initiated mating, and infected animals failed to reproduce despite increased sexual activity. Although detailed neuroanatomic studies were not performed, the syndrome was interpreted to be due to neuropathological changes in the limbic system.

E. Nonhuman Primates

The only reported studies of experimentally infected primates employed adult rhesus macaques (Macaca mulatta). These animals were initially hyperactive and subsequently became apathetic and hypokinetic. Pathology was remarkable for meningoencephalitis and retinopathy. Recent preliminary data suggest that a subtle or subclinical infection can be achieved in monkeys by neonatal intranasal infection.

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