Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Borna disease is a virus-induced, immunopathological encephalomyelitis in which CD4+ cells and macrophages dominate the pathological picture. However, significant numbers of CD8+ cells have been morphologically identified in perivascular infiltrates as well. To determine the contribution of different T-cell subsets to the pathogenesis of Borna disease, virus-infected rats were treated with monoclonal antibodies specific for CD4+ and CD8+ cells. Both types of monoclonal antibodies were able to significantly decrease or even prevent the local inflammatory reaction in the brain if given early during the infection. However, CD8-specific monoclonal antibodies appeared to be more effective than antibodies directed against CD4+ cells. Treatment initiated 4 days postinfection did not result in inhibition of encephalitis and disease. Virus titers in the brain of infected rats treated with T-cell-specific antibodies did not differ from titers in untreated infected control animals. The results indicate an important functional role of CD8+ cells, in addition to CD4+ cells, in the pathogenesis of Borna disease.
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PMID:Preventive effects of early anti-CD4 or anti-CD8 treatment on Borna disease in rats. 137 5

Borna disease is a virus-induced, immune-mediated encephalomyelitis based on a delayed-type hypersensitivity reaction. The severity of clinical symptoms after intracerebral infection of rats with Borna disease virus was reduced after treatment with transforming growth factor (TGF-beta 2). Intraperitoneal injection of the recombinant molecule, rTGF-beta 2, started on the day of infection at a dose of either 1 micrograms given every day or every other day for 8 consecutive days or 2 micrograms every third day, was found to result in the absence of typical Borna disease symptoms at 14 days after infection in most of the TGF-beta-treated rats, a time point at which all infected control animals not treated with rTGF-beta 2 showed distinct signs of Borna disease. The inhibition of the disease was paralleled by a significant reduction of the inflammatory reaction in the brain. However, the efficacy of treatment with rTGF-beta 2 was transient, because after day 21 only a slight or no reduction of the inflammatory reaction and, consequently, symptoms of Borna disease could be observed. Immunohistologic investigations revealed reduced CD4+ T cell numbers and no changes in macrophage counts in encephalitic lesions of rTG-beta treated rats. However, CD8+ cells were markedly decreased in the encephalitic lesions. Furthermore, the expression of MHC class II Ag was significantly reduced in the brain of rTGF-beta 2 treated Borna disease virus-infected rats, whereas MHC class I Ag expression was not. Most treated animals showed a reduction of Borna disease virus-specific serum antibodies, the result of an inhibition of the IgG response. The results presented here suggest a distinct influence of rTGF-beta 2 on T cell-mediated immune functions during the early phase of Borna disease virus-induced encephalomyelitis.
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PMID:Transforming growth factor-beta modulates T cell-mediated encephalitis caused by Borna disease virus. Pathogenic importance of CD8+ cells and suppression of antibody formation. 194 Mar 57

Borna disease (BD) virus, a still unclassified neurotropic agent, causes either fatal encephalomyelitis or persistent asymptomatic infection in a variety of animal species. We monitored the neuronal functions of intracerebrally infected but healthy rats with three types of learning experiments. Spatial discrimination learning, using the y maze and the hole board, was significantly less successful in BD virus-infected (I) compared with mock-infected (M) rats. Similarly, I rats tended to show a certain emotional disturbance (reduced resting behavior and less anxiety) as evaluated by open-field and neophobia tests. Furthermore, in two aversive learning experiments (taste aversion and reaction suppression via Skinner box), it appeared that the I rats expressed a significantly diminished ability to learn pain avoidance compared with M rats. In conclusion, we found specific learning deficiencies together with subtle behavioral alterations suggesting that BD virus causes certain modulations of high integrative brain functions which are only detectable under experimental conditions.
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PMID:Learning deficiencies in Borna disease virus-infected but clinically healthy rats. 251 30

Borna disease is an endemic progressive encephalomyelitis of horses and sheep prevalent in central Europe. A wide variety of animal species, ranging from chickens to primates can be infected experimentally with the causative virus, which is only poorly characterized. Furthermore, BD virus-specific antibodies have been detected in sera and cerebrospinal fluids of psychiatric patients. Our studies on the pathogenesis of BD have shown that-at least in rats-the disease is not caused by the infecting virus itself, but by a virus-induced immunopathological reaction. Thus, after intracerebral infection immunoincompetent rats do not get the disease despite persistent virus replication in cells of the central nervous system. However, after adoptive transfer of immune cells from diseased rats, immunoincompetent rats exhibit full-blown BD. Recently, we have been successful in establishing a virus-specific T cell line of the helper/inducer phenotype (CD4+). This T cell was shown to play an important role in the pathogenesis of BD, suggesting that the disease is caused by a delayed type hypersensitivity reaction.
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PMID:Immune-mediated pathogenesis of Borna disease. 326 62

Borna disease occurs naturally in horses and sheep and causes an encephalomyelitis which is fatal. Little is known about the etiologic agent. There is evidence, however, that this neutrotropic virus belongs to the conventional enveloped RNA viruses. Experimentally infected rabbits exhibited a highly reproducible multifocal retinochoroidopathy. Clinical, histologic, as well as virologic results suggested that immunologic events gave rise to the characteristic clinical, histologic, as well as virologic results suggested that immunologic events gave rise to the characteristic clinical expression of the disease. To investigate possible immunpathologic factors, infected rabbits were treated with immunosuppressive drugs. As compared with controls three outstanding features were observed in the treated group: (1) The time interval between infection and the occurrence of inflammatory ocular foci was considerably prolonged; (2) confluency of retinal lesions was not noted in the early course of the disease; and (3) a lack of ocular lesions or a nonprogression over several days, never observed in controls, occurred in a small percentage of treated animals. These observations indicate that the clinical course of virus-induced inflammatory lesions of the retina and choroid can be changed by treatment with immunosuppressive drugs. It can be assumed that the appearance of the individual fundus lesion depends on the immuno-logic status of the infected host.
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PMID:Borna disease virus-induced retinouveitis treated with immunosuppressive drugs. 691 Mar 49

Borna disease, a naturally occurring encephalomyelitis of horses and sheep, was induced in rhesus monkeys after intracerebral infection with virus containing rabbit brain suspension. The animals developed neurological disorders followed by a severe encephalomyelitis which was accompanied by a retinopathy. In all the analyzed brain and retina tissue pieces, virus-specific antigen could be demonstrated by immunoelectrophoretic techniques. Antibodies could be demonstrated by the intermediate gel technique as well as by the immunofluorescence test in the serum and the cerebrospinal fluid of all the monkeys. The histopathological findings in the brain and the eye might be comparable to certain types of encephalitis in man and to pathological changes in the eye of human patients, the etiologies of which are still obscure. An attempt was also made to study cell-mediated immunity by a chromium release assay in infected animals, the results of which might provide, together with the histopathological observations, strong evidence for the role of lymphocytes in the pathogenesis of BD infection in rhesus monkeys.
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PMID:Borna disease in rhesus monkeys as a models for uveo-cerebral symptoms. 724 Oct 97

In situ hybridization, RT-PCR and Northern blot analysis as well immunohistochemistry were used to examine the expression of C1q, a subcomponent of the rat complement system, in brains of rats infected with Borna disease virus (BDV) and rats afflicted with experimental allergic encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein specific T cells. C1q mRNA, which was not detected in normal brain, became clearly detectable using RT-PCR analysis by d14 post infection (p.i.) with BDV. Maximal levels of C1q mRNA were reached 21 days p.i. when inflammatory reactions in the brain were also at a peak. Similarly, C1q mRNA was elevated when the clinical symptoms of EAE became evident 5 days following cell transfer. C1q positive cells, as identified by immunohistology, were preferentially localized in grey and white matter of the hippocampus and basolateral cortex. The C1q positive cells resembled microglial cells in morphology. The correlation of C1q expression with the development of neurological disease as well as the dramatic increase of C1q within brain regions with inflammatory lesions suggest that local biosynthesis of C1q may play a role in the pathogenesis of Borna virus induced and autoimmune encephalomyelitis.
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PMID:Expression of C1q, a subcomponent of the rat complement system, is dramatically enhanced in brains of rats with either Borna disease or experimental allergic encephalomyelitis. 754 1

A Borna disease virus (BDV)-like agent was isolated from the central nervous system (CNS) of cats with a spontaneous non-suppurative encephalomyelitis ('staggering disease'). In contrast to the rabbit-adapted BDV strain V, which can be propagated in several primary and permanent cell cultures, the cat virus grew only in embryonic mink brain cells. Infection of adult Wistar rats with feline brain tissue material did not result in clinical disease during a period of 5 months, nor in growth of infectious virus in the brain. However, using the brain suspension of a newborn rat inoculated with feline brain tissue material, it was possible to induce typical Borna disease (BD) in four adult rats. This indicates a possible adaptation of the cat virus during passages in rats. By the use of an RT-PCR technique, BDV-specific RNA could be detected in a majority of brain samples from diseased cats. BDV-specific antigen was demonstrated in feline CNS samples both by immunohistochemistry and ELISA. However, the amount of BDV RNA and BDV antigen was less in the cats as compared to horses with BD, providing further support for the notion that a distinct feline BDV strain exists.
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PMID:Staggering disease in cats: isolation and characterization of the feline Borna disease virus. 756 58

Borna disease represents a unique model of a virus-induced immunological disease of the brain. Naturally occurring in horses and sheep, the mechanisms of pathogenesis have been studied in experimental animals, namely in the rat. Many investigations have revealed that the infection of the natural hosts principally follows the same pathogenic pathways as observed in rats, leading to a severe encephalomyelitis. This affliction of the central nervous system results in severe neurological disorders that again, are fully comparable in laboratory animals to those in the natural and the different experimental hosts. In addition, alterations have been reported which are also based on the infection of the brain and do not result in the classical encephalitic clinical picture but rather in alterations of behavior. However, to all of our knowledge, the various clinical pictures of Borna disease are not caused by the infecting virus itself but rather by the hosts immune response towards it, i.e. by a virus-induced cell-mediated immunopathological reaction. The importance of virus-specific CD4+ T cells as exemplified by a cultured T cell line and of CD8+ T cells as shown by immunomodulatory substances and specific antibody treatment in vivo for the pathogenesis of acute Borna disease will be elucidated here. In addition, evidence will be provided that virus-specific CD8+ T cells are also responsible for the dramatic brain atrophy in the chronic phase of the disease in rats. Therefore, Borna disease not only lends itself exquisitely well to the study of the pathogenesis of an immunopathological disease of the brain but also represents one of the few models for immune-mediated tissue destruction that eventually leads to brain atrophy and clinically to dementia.
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PMID:Pathogenesis of Borna disease. 821 98

Borna disease (BD) is a naturally occurring enzootic encephalomyelitis of horses and sheep. The aetiological agent, Borna disease virus (BDV) is an unclassified, neurotropic, negative stranded RNA virus. The study aimed at providing further information on BD of naturally infected animals. Samples obtained from 20 animals (18 horses, 1 donkey, 1 sheep) were investigated by a series of virological and molecular biological tests. The highly sensitive reverse transcription-polymerase chain reaction (RT-PCR) method was used to analyze the tissue distribution of BDV-specific RNA. BDV-specific RNA was detected in bulbus olfactorius, nucleus caudatus, hippocampus and cerebral cortex of all infected animals. BDV-RNA was also present in the spinal cord, eye, nasal mucosa, parotide gland, lung, heart, liver, kidney, bladder and ovaries. In addition, BV-specific RNA was also detected in conjunctival fluid, nasal secretions and saliva of two infected animals. By Western Blot assays the highest amounts of BDV antigens were demonstrated in bulbus olfactorius, nucleus caudatus, hippocampus and cerebral cortex.
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PMID:[Distribution of Borna disease virus in naturally infected animals with clinical disease]. 869 47


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