Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Borna disease is a naturally occurring meningoencephalomyelitis of sheep and horses. After experimental infection of rats with Borna disease virus a biphasic disease with initial gait disturbances and later paresis and paralysis can be observed. The disease symptoms in these experimental animals resemble those of the natural hosts. The disease is not caused by the infecting virus itself but rather by a CD4+ T cell-mediated immune response. After the pathogenesis had been elucidated new strategies for the therapy of Borna disease by interfering with the immune reaction have been developed. Treatment with immunosuppressive drugs, with monoclonal antibodies directed against certain immune cells and with mediators of the immune reaction resulted in an inhibition or significant reduction of Borna disease symptoms.
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PMID:[Immune intervention in Borna disease]. 175 66

A spontaneous neurological disease in domestic cats is described. The clinical signs included staggering gait, hind limb ataxia, and paresis. Histologically, a nonsuppurative meningoencephalomyelitis with a characteristic distribution pattern was found, indicating a viral etiology. In serum samples from diseased cats, antibodies to Borna disease virus were demonstrated.
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PMID:Description of feline nonsuppurative meningoencephalomyelitis ("staggering disease") and studies of its etiology. 765 Feb 12

Borna disease is an immunopathological virus-induced encephalopathy comprising severe inflammation and degenerative brain cell lesions which results in organ atrophy and chronic debility in rats. CD4+ and CD8+ T cells have been reported to be involved in the development of this disease of the central nervous system. A virus-specific homogeneous T-cell line, established in vitro after immunization of rats with the recombinant 24-kDa virus-specific protein, showed antigen-specific proliferation in the presence of the 24-kDa but not the 38-kDa Borna disease virus-specific protein, another major virus-specific antigen. This T-cell line, P205, was found to exhibit characteristics of a T-helper cell: CD4+ CD8- IL-2- IL-4- IFN-gamma+ IL-6+ IL-10+. Furthermore, this T-cell line expressed the alpha/beta T-cell receptor and the alpha 4 integrin (VLA-4). Adoptive transfer of this helper cell resulted in an increase of antibody titers and two different types of disease in virus-infected rats after cyclophosphamide-induced immunosuppression. (i) Rats receiving T cells between 10 and 18 days after treatment with cyclophosphamide showed an acute lymphoproliferative disease in the gut and lungs within 9 days after adoptive transfer and died. (ii) Passive transfer within the first 5 days after immunosuppressive treatment resulted in typical Borna disease associated with neurological symptoms such as ataxia and paresis starting 14 to 16 days after transfer. Immunohistological analysis of the brains of rats with Borna disease uniformly revealed the presence of CD8+ T cells in encephalitic lesions in addition to CD4+ cells that were found in the brains of recipients of the virus-specific CD4+ T-cell line, irrespective of whether neurological symptoms developed or not. However, recipient rats treated with antibodies against CD8+ T cells developed neither encephalitis nor disease. Therefore, CD4+ T cells appear to accumulate in the brain and cause perivascular inflammatory lesions which alone obviously do not cause disease. In contrast, the presence of CD8+ cells apparently directly correlates with the development of neurological symptoms.
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PMID:Immunopathogenic role of T-cell subsets in Borna disease virus-induced progressive encephalitis. 781 58

Necropsy records and causes of mortality of ostriches up to 3 months old over a 5-year period (1989-1993) are presented. The data relate to one ostrich enterprise that comprises 10 breeding flocks, five rearing farms, and one hatchery. Causes of mortality are classified into nine major categories. The annual mortality percentages of all hatched ostriches over the 5-year period were 61%, 58%, 30%, 29%, and 16.6%, and the most significant cause of death was a paresis syndrome that accounted for 20%, 11%, 16%, 10.1%, and 2% mortality, respectively. Limb deformities and gastroenteritis were the other principal specific causes of mortality. The paresis syndrome was caused by an agent serologically related to Borna disease virus. Brain extracts from paralyzed ostriches, when given orally or intramuscularly to 5-week-old birds, reproduced the clinical signs and microscopic lesions. The mean time to death was less than 3 weeks for the intramuscularly infected group and was almost twice as long for the orally infected group.
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PMID:Causes of losses including a Borna disease paralytic syndrome affecting young ostriches of one breeding organization over a five-year period (1989-1993). 871 43

A pregnant mare showing pyrexia, reduced appetite, ataxia and paresis was euthanized and examined for the presence of Borna disease virus (BDV). Her brain, showing multiple neuronal degeneration and necrosis with hemorrhage, and the histologically normal brain of the fetus were both positive for BDV RNA. The BDV nucleotide sequences were identical in the mare and fetus in the second open reading frame (ORF). This is the first report of the possible vertical transmission of BDV in a horse.
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PMID:Detection of Borna disease virus in a pregnant mare and her fetus. 1072 31

Numerous cases of acute-onset progressive ataxia, hindlimb paresis and paralysis of unknown aetiology occurred during 1993 to 2003 in cheetahs (Acinonyx jubatus) within the European Endangered Species Programme (eep). This study describes the immunohistochemical investigation of a possible viral aetiology of the "cheetah myelopathy". Antibodies to feline herpesvirus type 1, canine distemper virus, canine parvovirus and Borna disease virus were applied to formalin-fixed and paraffin-embedded brain and spinal cord sections from 25 affected cheetahs aged between three-and-a-half months and 13 years. Using the avidin-biotin complex technique, none of the antibodies gave positive immunosignals in either the brain or the spinal cord tissue.
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PMID:Immunohistochemical screening for viral agents in cheetahs (Acinonyx jubatus) with myelopathy. 1705 52