Neonatal Borna disease virus infection in the rat causes a loss of Purkinje cells in the cerebellum

Citation
Lm. Eisenman et al., Neonatal Borna disease virus infection in the rat causes a loss of Purkinje cells in the cerebellum, J NEUROVIRO, 5(2), 1999, pp. 181-189
Citations number
44
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROVIROLOGY
ISSN journal
13550284 → ACNP
Volume
5
Issue
2
Year of publication
1999
Pages
181 - 189
Database
ISI
SICI code
1355-0284(199904)5:2<181:NBDVII>2.0.ZU;2-T
Abstract
Viral insults that occur during early postnatal periods, can affect neurona l systems which exhibit significant postnatal development, such as the cere bral cortex and cerebellum Borna disease virus (BDV) is a single-strand RNA virus which replicates in the nervous system of many species after experim ental inoculation and causes acute neurological disease. Neonatal rats infe cted with BDV do not mount an aggressive response to the virus like their a dult counterparts, but instead develop a persistent BDV infection with less overt clinical sequelae. Recently, the cerebellum, a neural structure asso ciated with regulation of motor behavior, and perhaps with higher cognitive functions, has been demonstrated to be a target of neonatal BDV infections in rats (Bautista ct al, 1995). In the present study neonatal rats were in fected with BDV and their cerebella were analyzed histologically and - immu nohistochemically at 7 months of age. The cerebella of infected animals wer e reduced in size but normal foliation and laminar organization was present . However, as visualized with immunohistochemistry for the Purkinje cell-sp ecific antigen calbindin, there were numerous gaps within the Purkinje cell layer and in the molecular layer which contains the Purkinje cell dendriti c trees. We estimated the number of Purkinje cells and found there was an a pproximately 75% loss of PC in adult rats neonatally infected with BDV. The se results suggest that neonatal BDV infection may either (1) target the PC and cause the death of these cells directly or (2) acts indirectly by trig gering an immune response which is then responsible for the loss of these c ells.