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)

Chronic Theiler's murine encephalomyelitis virus infection of susceptible mice is an animal model for human demyelinating diseases. Previously we described an altered and diminished pattern of central nervous system disease in immunocompetent SJL/J mice infected with a variant virus. This variant virus H7A6-2 was selected with a neutralizing mAb recognizing the capsid protein VP-1 of Theiler's virus. Here we characterize the variant virus by ELISA and neutralization assays and by sequencing selected regions of the viral RNA genome and relate the alteration to disease. The variant virus contains one single point mutation within a neutralizing epitope of VP-1. This nucleotide change lead to an amino acid replacement at amino acid 101 of VP-1, a threonine (wild type) to an isoleucine (variant). Model building based on sequence alignments and the known structure of the related Mengo virus indicates that the altered amino acid is located in an exposed loop on the surface of the virus at the periphery of a site that has been proposed to be the receptor binding site. The results of ELISA, neutralization assay, and direct RNA sequencing provide for the first time an opportunity to precisely map an important structural determinant of neurovirulence.
J Exp Med 1989 Dec 01
PMID:Alteration of amino acid 101 within capsid protein VP-1 changes the pathogenicity of Theiler's murine encephalomyelitis virus. 247 6

Two synthetic immunodominant and nonencephalitogenic peptides of myelin basic protein, N1-20 and AcN9-20, effectively compete with an encephalitogenic peptide, AcN1-11, in an in vitro T-cell response restricted by class II major histocompatibility complex products (I-Au). These mutant peptide constructs, which do not occur in nature, also compete with the self-antigen for the in vivo induction of T cells primed with the encephalitogen AcN1-11. By using these nonpathogenic competitor peptides, it is possible to prevent the development of a prototypic T-cell-mediated autoimmune disease, experimental allergic encephalomyelitis. These results suggest possibilities for the utilization of competitor peptides for therapy of T-cell-mediated autoimmune diseases linked to specific major histocompatibility complex genes.
Proc Natl Acad Sci U S A 1989 Dec
PMID:Prevention of experimental encephalomyelitis with peptides that block interaction of T cells with major histocompatibility complex proteins. 248 Jun 2

Multiple sclerosis is a demyelinating disease of the central nervous system with genetic, viral and autoimmune characteristics. Myelin basic protein (MBP) is a suspected target autoantigen since it induces experimental autoimmune encephalomyelitis, an animal model closely resembling multiple sclerosis. The disease is mediated by Class II restricted, MBP-reactive T cells possessing the T helper/inducer phenotype. In the present study, we have isolated MBP-reactive T cell clones from the peripheral blood of a chronic progressive multiple sclerosis patient. The clones displayed blastogenic memory responses when rechallenged with the autoantigen and irradiated autologous lymphocytes. MBP recognition by the autoantigen-reactive T lymphocytes was restricted by major histocompatibility complex Class II antigens. Both CD4+8- and CD4-8+ MBP-reactive T cell clones were obtained.
J Immunogenet 1989 Dec
PMID:MHC-restricted autoantigen-reactive T cell clones in multiple sclerosis. 248 13

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.
Biol Psychiatry 1989 Dec
PMID:Learning deficiencies in Borna disease virus-infected but clinically healthy rats. 251 30

Acute monophasic experimental autoimmune encephalomyelitis (AMEAE) was induced in 5 Macacus cynomolgus monkeys. Serum and cerebrospinal fluid (CSF) paired samples were collected before and four weeks after immunization, time of complete development of AMEAE clinical picture. After immunization the CSF/serum albumin ratio and the IgG index were markedly increased. Agarose isoelectric focusing (AIEF) followed by immunofixation revealed faint IgG oligoclonal bands in both serum and CSF of all monkeys, which became more evident after Kappa and Lambda assessment. Intrathecal synthesis of IgG oligoclonal bands was detected in only one CSF. Affinity-driven immunoblotting failed to detect anti-myelin basic protein (MBP) oligoclonal IgG. No free light chain (FLC) patterns or IgA and IgM oligoclonal bands were detected.
Ital J Neurol Sci 1989 Dec
PMID:Experimental allergic encephalomyelitis in the monkey: humoral immunity and blood-brain barrier function. 251 67

A 3-wk-old lamb died because of neurological disease. The predominant microscopic lesions were in the brain and spinal cord and consisted of nonsuppurative encephalomyelitis with severe gliosis throughout the gray and white matter. Immature and mature schizonts, 15.7 x 10.6 microns (8-30 x 6-18 microns), occurred in capillaries and were structurally similar to those of Sarcocystis tenella.
J Parasitol 1989 Dec
PMID:Fatal perinatal sarcocystosis in a lamb. 251 65

To investigate polyprotein processing of Theiler's murine encephalomyelitis viruses, we analyzed in vitro translation reactions programmed by in vitro-derived transcripts from an infectious full-length cDNA clone of the DA strain of Theiler's virus. To help identify the proteinases that carried out the processing, we modified the DA cDNA clone transcription template by linearization with different restriction endonucleases that generate templates of different lengths or by constructing linker insertion or deletion mutations or both in putative proteinase-coding regions. Protein 3C carried out most of the cleavages of the polyprotein, as is true for the other picornaviruses that have been studied. A second proteinase also appeared active at the LP12A-2B junction. A protein of slightly faster mobility than the leader protein was seen with translation of transcripts derived from DA cDNA but not GDVII cDNA. This protein may be synthesized from an alternative initiation site in the DA leader-coding region out of phase with the polyprotein reading frame. Our findings are relevant to ongoing investigations of the abnormal virus expression seen in DA virus late demyelinating disease, since polyprotein processing is critical in regulating picornaviral gene expression.
J Virol 1989 Dec
PMID:Polyprotein processing of Theiler's murine encephalomyelitis virus. 255 59

The DA strain and other members of the TO subgroup of Theiler's murine encephalomyelitis viruses cause a persistent demyelinating infection, whereas the GDVII strain and other GDVII subgroup strains cause an acute lethal polioencephalomyelitis. We generated an infectious DA cDNA clone inserted into a transcription vector. Virus derived from transfection of transcripts produced a demyelinating disease indistinguishable from that of wild-type virus. The infectious clone provides a critical reagent for the production of interstrain recombinant viruses to help identify genetic loci responsible for the biological activities of the strains.
J Virol 1989 Dec
PMID:Infectious cDNA clones of the DA strain of Theiler's murine encephalomyelitis virus. 255 69

Using localized proton spectroscopy, the author and associates previously have observed an increase in the resonance at 1.2 +/- 0.2 ppm in the brain of monkeys with experimental allergic encephalomyelitis (EAE). In proton nuclear magnetic resonance (NMR) spectroscopy, the lactate methyl protons resonate at dose to the same chemical shift frequency as the lipid methylene protons (1.2 +/- 0.2 ppm). Noninvasive zero quantum NMR techniques were used to separate lipids from lactate in the brain during the course of EAE development. Out of 53 zero quantum NMR measurements (from three animals), 16 measurements were made at a time when a resonance at 1.2 ppm appeared (after the animals developed EAE). In all these cases, lactate was not detectable. The fact that the resonance (identified as lipids with zero quantum techniques) correlated with histochemical Oil red O staining suggests that these mobile NMR signals are associated with demyelination.
Invest Radiol 1989 Dec
PMID:Separation of lipids from lactate in experimental allergic encephalomyelitis by zero quantum NMR techniques. 255 87

Treatment with the beta-adrenergic agonist isoproterenol suppresses clinical and histological experimental allergic encephalomyelitis in Lewis rats. The effect of isoproterenol treatment is greater when the drug is given from the time of immunization through the acute phase of the illness or from 8 to 14 days post-immunization than when given for the first 7 days after immunization.
J Neuroimmunol 1989 Dec
PMID:The beta-adrenergic agonist isoproterenol suppresses experimental allergic encephalomyelitis in Lewis rats. 257 18


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