Experimental Infection: Pathogenesis of Neurobehavioral Disease

Abstract

Even though findings obtained from experimental Borna disease virus (BDV) infection of other species gave many insights into species-specific pathogenic processes, BDV infection of the rat is the most common model for studying the pathogenesis of Borna disease (BD). In infections in which MHC class II-restricted cytotoxic T-cell activity was elicited in vitro, there has been no direct evidence for in vivo antiviral effector cell lysis. Thus, it was interesting that initial reports suggested that CD4+ cells played the major role in the immunopathogenesis of BDV. Investigations of experimental adult BDV infection in other species replicated findings from the rat model and extended one's understanding of the pathogenesis of BD. Viral infections of the central nervous system (CNS) are a significant cause of congenital disease in newborns. Moreover, many neuropsychiatric disorders of children, such as autism, may result from early brain injury during critical periods of pre- or postnatal brain development. The hippocampal formation, especially neurons of the CA3 and CA4 areas, is one of the first targets of neonatal BDV infection. Damage to the cerebellum has also been observed in other perinatal virus infections, including lymphocytic choriomeningitis virus, rubella, mumps, rat parvovirus, or reovirus type III. The study of the pathogenesis of neurological diseases caused by BDV infection is a formidable challenge. Importantly, during the asymptomatic phase of the disease, the virus replication was predominantly detected in the cerebral cortex and hippocampus.