Borna disease virus-induced meningoencephalomyelitis caused by a virus-specific CD4+ T cell-mediated immune reaction

Richt, Jürgen A.; Stitz, Lothar; Deschl, Ulrich; Frese, K.; Rott, R.

doi:10.1099/0022-1317-71-11-2565

Cited by 54 publications

(65 citation statements)

References 32 publications

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“…Pathological lesions in the CNS consisted of perivascular infiltrates in which macrophages and T lymphocytes ( Fig. 2 and 3) were dominant in accordance with previous findings (Deschl et aL, 1990;Richtet al, 1990). Enlargement of cerebral ventricles began around day 50 and later developed into hydrocephalus (Narayan et al, 1983b).…”

Section: Resistance Of Bh Rats To Borna Diseasesupporting

confidence: 78%

“…Since T cells were found to play a significant role in the pathogenesis of BD in LEW rats (Rott et al, 1988;Richt et al, 1989Richt et al, , 1990 we studied first the influence of MHC on the susceptibility by infection of a panel of RT1 congenic strains having a BH or LEW background. Our results clearly document that the difference between LEW and BH rats is not related to the variant RT1 genes, in which these strains differ.…”

Section: Discussionmentioning

confidence: 99%

“…For routine histology 5 ~tm sections were stained with haematoxylin and eosin; for immunocytochemical labelling of macrophages the monoclonal anti- body (MAb) Edl (kindly provided by Dr Dijkstra, Utrecht, The Netherlands) and for demonstration of T lymphocytes the MAb W3/13 (SeroTec) were used as described previously (Deschl et al, 1990).…”

Section: Histopathology and Immunocytochemistrymentioning

confidence: 99%

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Studies on the genetic control of resistance of black hooded rats to Borna disease

Herzog

Frese

Rott

1991

Journal of General Virology

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In contrast to Lewis (LEW) and Wistar rats, black hooded (BH) rats inoculated with Borna disease (BD) virus developed neither encephalitis nor clinical disease despite persistent replication of the virus in the central nervous system. In comparison to LEW rats, production of virus-specific antibodies was significantly delayed in BD-resistant BH rats, even though identical titres were finally reached. The different susceptibility in LEW and BH rats was studied further by investigating responses of F~ hybrid animals. Although these rats developed encephalitis, they did not become sick. The differences in host responses for BD virus were found to be genetically determined but were independent of class I or class II major histocompatibility complex gene products or to genes responsible for lymphocyte differentiation.

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Section: Resistance Of Bh Rats To Borna Diseasesupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Histopathology and Immunocytochemistrymentioning

confidence: 99%

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Studies on the genetic control of resistance of black hooded rats to Borna disease

Herzog

Frese

Rott

1991

Journal of General Virology

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“…The results of these studies are highly controversial in either identifying or failing to detect evidence of BDV infection in peripheral blood cells and brain tissue from psychiatric patients (Bode et al, 1995;Kishi et al, 1995a,b;Richt et al, 1990). Evidence supporting this notion of an association between BDV and psychiatric illness also comes from studies which show disturbances in the catecholamine system in rats infected with BDV (Solbrig et al, 1996a, b).…”

Section: Introductionmentioning

confidence: 88%

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

et al. 1999

J Neurovirol

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Viral insults that occur during early postnatal periods, can affect neuronal systems which exhibit signi®cant postnatal development, such as the cerebral cortex and cerebellum. Borna disease virus (BDV) is a single-strand RNA virus which replicates in the nervous system of many species after experimental inoculation and causes acute neurological disease. Neonatal rats infected with BDV do not mount an aggressive response to the virus like their adult counterparts, but instead develop a persistent BDV infection with less overt clinical sequelae. Recently, the cerebellum, a neural structure associated 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 et al, 1995). In the present study neonatal rats were infected with BDV and their cerebella were analyzed histologically and immunohistochemically at 7 months of age. The cerebella of infected animals were reduced in size but normal foliation and laminar organization was present. However, as visualized with immunohistochemistry for the Purkinje cell-speci®c antigen calbindin, there were numerous gaps within the Purkinje cell layer and in the molecular layer which contains the Purkinje cell dendritic trees. We estimated the number of Purkinje cells and found there was an approximately 75% loss of PC in adult rats neonatally infected with BDV. These 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 triggering an immune response which is then responsible for the loss of these cells.

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“…In the developing rat, BDV infection causes a slow, progressive loss of Purkinje cells, with limited neuropathological and behavioral changes and little evidence of CNS inflammation (9,10). On the other hand, the acute Borna disease seen in immunocompetent adult rats is associated with extensive CD4 T cell-dependent CNS inflammation and BDV-specific CD8 T cell activity (11)(12)(13)(14)(15). Levels of mRNA for IL-1␣, IL-2, IL-6, TNF-␣, and IFN-␥ as well as other immunologically relevant factors all become elevated in the brains of rats acutely infected with BDV (16 -19).…”

mentioning

confidence: 99%

The Central Nervous System Inflammatory Response to Neurotropic Virus Infection Is Peroxynitrite Dependent

Hooper

Kean

Scott

et al. 2001

The Journal of Immunology

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We have recently demonstrated that increased blood-CNS barrier permeability and CNS inflammation in a conventional mouse model of experimental allergic encephalomyelitis are dependent upon the production of peroxynitrite (ONOO−), a product of the free radicals NO· and superoxide (O2·−). To determine whether this is a reflection of the physiological contribution of ONOO− to an immune response against a neurotropic pathogen, we have assessed the effects on adult rats acutely infected with Borna disease virus (BDV) of administration of uric acid (UA), an inhibitor of select chemical reactions associated with ONOO−. The pathogenesis of acute Borna disease in immunocompetent adult rats results from the immune response to the neurotropic BDV, rather than the direct effects of BDV infection of neurons. An important stage in the BDV-specific neuroimmune response is the invasion of inflammatory cells into the CNS. UA treatment inhibited the onset of clinical disease, and prevented the elevated blood-brain barrier permeability as well as CNS inflammation seen in control-treated BDV-infected rats. The replication and spread of BDV in the CNS were unchanged by the administration of UA, and only minimal effects on the immune response to BDV Ags were observed. These results indicate that the CNS inflammatory response to neurotropic virus infection is likely to be dependent upon the activity of ONOO− or its products on the blood-brain barrier.

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Borna disease virus-induced meningoencephalomyelitis caused by a virus-specific CD4+ T cell-mediated immune reaction

Cited by 54 publications

References 32 publications

Studies on the genetic control of resistance of black hooded rats to Borna disease

Studies on the genetic control of resistance of black hooded rats to Borna disease

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

The Central Nervous System Inflammatory Response to Neurotropic Virus Infection Is Peroxynitrite Dependent

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