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)

To study T cell and macrophage activity during measles, levels of interferon-gamma (IFN-gamma) and neopterin in plasma and cerebrospinal fluid (CSF) were measured. Plasma levels of IFN-gamma were elevated in measles (1.17 +/- 0.27) compared with healthy adults (0.13 +/- 0.06, P less than .05) and children (0.14 +/- 0.06, P less than .01). Plasma levels of neopterin were elevated in measles (32.5 +/- 2.7) compared with healthy adults (5.3 +/- 2.9, P less than .0001), healthy children (12.1 +/- 4.0, P less than .001), and children with other infectious diseases (20.6 +/- 4.0, P less than .02). IFN-gamma was increased in measles primarily during rash; neopterin remained elevated for several weeks. Levels of neopterin showed a significant positive correlation with plasma levels of soluble interleukin-2 receptor and soluble CD8, two other parameters of T cell activation. Children with measles complicated by pneumonia had higher levels of neopterin in serum than those with uncomplicated disease. Children with measles complicated by autoimmune encephalomyelitis had higher levels of neopterin in CSF than those with noninflammatory neurologic disease but lower than those with central nervous system infections. Thus, IFN-gamma seems to be produced in vivo during acute measles virus infection; deficiency of this lymphokine does not appear to correlate with increased susceptibility to secondary infections.
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PMID:Immune activation during measles: interferon-gamma and neopterin in plasma and cerebrospinal fluid in complicated and uncomplicated disease. 210 64

A patient with atypical manifestations of Epstein-Barr Virus (EBV) encephalomyelitis is presented. The patient had unusual spinal fluid immunoglobulin abnormalities, the syndrome of inappropriate anti-diuretic hormone secretion, autonomic dysfunction and spinal arachnoiditis. The cisternal CSF, with a very high IgG level (34.3 mg/dl; normal less than 6.1) but a normal albumin content, displayed evidence of massive intrathecal immunoglobulin production. This was further confirmed by the presence of oligoclonal bands. These clinical manifestations have not previously been reported in encephalomyelitis associated with EBV infection.
Infection
PMID:Unusual manifestations of Epstein-Barr virus encephalomyelitis. 184 3

Wild turkeys (Meleagridis gallopavo silvestris) trapped as part of a relocation program by the Arkansas Game and Fish Commission were tested for selected infectious diseases and parasites. The 45 birds were trapped at four locations in Pope, Scott, and Montgomery counties (Arkansas, USA). Forty-four blood samples for serology, 27 blood smears and 12 fecal samples were collected. Of the serum samples tested, 20 of 44 (45%) were positive for Pasteurella multocida by enzyme-linked immunosorbent assay (ELISA), 42 of 44 (95%) were positive for Bordetella avium by ELISA, and 15 of 44 (34%) were positive for Newcastle disease virus antibody by the hemagglutination inhibition test. All serum samples were negative for Mycoplasma gallisepticum, Mycoplasma synoviae, avian paramyxovirus 3, avian influenza, hemorrhagic enteritis, Marek's disease, avian encephalomyelitis, laryngotracheitis, Salmonella pullorum and Salmonella gallinarum. Haemoproteus meleagridis was found in eight of 27 (30%) and Leucocytozoon smithi in nine of 27 (33%) blood smears; all smears were negative for Plasmodium hermani. Enteric parasites included Ascaridia dissimilis, Heterakis gallinarum, Eimeria dispersa and Raillietina spp. This study was an attempt to document the health status and disease exposure of wild turkeys in Arkansas to aid in managing and preventing the spread of disease agents to wild turkeys and other species of birds.
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PMID:A survey of infectious diseases in wild turkeys (Meleagridis gallopavo silvestris) from Arkansas. 225 Mar 23

Employing a murine model of multiple sclerosis which utilizes intracranial injection of Theiler's virus murine encephalomyelitis (TMEV) into SJL/J mice, we tested the potential role of tumor necrosis factor alpha (TNF-alpha) in ameliorating CNS demyelination. Infection with TMEV caused early grey matter inflammation (7 days post-infection) in the brain and spinal cord followed by chronic demyelination (35 days post-infection) in the spinal cord. Administration of recombinant human or mouse TNF-alpha starting 12 h prior to infection and then three times weekly had minimal effect on development of grey matter inflammation in the spinal cord. In contrast, TNF-alpha dramatically reduced demyelination present in spinal cord on days 14 and 35 after TMEV infection (P less than 0.01) when compared to controls. CNS virus titers of TMEV were not modified by TNF-alpha administration as measured on days 7, 14, and 35 following infection. In vivo administration of TNF-alpha inhibits TMEV-induced demyelination in susceptible SJL/J mice without affecting virus replication in the CNS.
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PMID:Inhibition of Theiler's virus-induced demyelination in vivo by tumor necrosis factor alpha. 227 4

Intracerebral inoculation of mice with Theiler's murine encephalomyelitis virus results in an intense inflammatory response of mononuclear leukocytes which infiltrate into the central nervous system. Resistant strains of mice have the ability to clear virus whereas susceptible strains become infected persistently and are associated with chronic demyelination which is proposed to be immune-mediated. In an attempt to better understand the role of the immune response during demyelination, mononuclear leukocytes were isolated from the central nervous system of infected mice and stained by an immunoperoxidase technique with anti-Thy-1.2, anti-L3T4, anti-Lyt-2 and anti-MAC-1 mAb. Infection of susceptible SJL/J mice resulted in a biphasic immune response which peaked on days 7 and 27 post-infection. In contrast, a single peak (day 7) was observed in resistant C57BL/10SNJ mice. The presence of Thy-1.2, L3T4, and MAC-1+ cells was similar between the two strains. However, although the number of Lyt-2+ cells peaked on day 7 in C57BL/10SNJ mice, they were not detected in SJL/J mice until 14 days post-infection and gradually increased in number over the course of infection. To further study the role of T cells in demyelination, serial frozen sections of brain and spinal cord were stained for the presence of Lyt-2 and L3T4+ cells in the lesions of chronically infected SJL/J mice. L3T4+ cells were observed predominantly in perivascular regions while Lyt-2+ cells were observed infiltrating the parenchyma. These results provide further evidence that Lyt-2+ lymphocytes are important in the mechanism of susceptibility/resistance to Theiler's murine encephalomyelitis virus-induced demyelination.
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PMID:Characterization of the inflammatory response in the central nervous system of mice susceptible or resistant to demyelination by Theiler's virus. 249 23

Measles is associated with alterations in immune regulation that sometimes lead to secondary infections or autoimmune encephalomyelitis. Simultaneously, an effective measles virus-specific immune response develops. To relate immune activation to measles and its complications, we studied the spontaneous proliferation of blood mononuclear cells and circulating levels of soluble interleukin-2 receptor and CD8 T-cell antigens in 126 patients with complicated or uncomplicated measles at various stages of the disease. Spontaneous proliferation of mononuclear cells, which was present through the first week of the rash, was greater in cells from patients with measles (8787 +/- 1403 cpm) than in those from healthy children (1529 +/- 237 cpm, P less than 0.0001). Levels of soluble interleukin-2 receptor (3385 +/- 195 units per milliliter) and CD8 (4145 +/- 437 units per milliliter) were higher in patients with measles than in those with other infectious diseases (2377 +/- 440, P = 0.003; 2399 +/- 771, P = 0.0374) or in healthy children (865 +/- 138, P less than 0.0001; 1026 +/- 169, P less than 0.0001). Levels of soluble interleukin-2 receptor were elevated before the onset of the rash and remained elevated for several weeks. In contrast, levels of soluble CD8 increased only when the rash appeared, and subsided quickly. Spontaneous proliferation of mononuclear cells and levels of soluble CD8 were similar in patients with uncomplicated disease, pneumonia, or encephalomyelitis, but soluble interleukin-2 receptor levels were lower in patients with encephalomyelitis (2312 +/- 314 vs. 3455 +/- 247 units per milliliter in uncomplicated measles; P = 0.01). In patients with encephalomyelitis, cerebrospinal fluid levels of soluble CD8 (686 +/- 350 units per milliliter), but not interleukin-2 receptor (9 +/- 8.3 units per milliliter), were increased. We conclude that the proliferative phase of the immune response, as measured by the release of soluble interleukin-2 receptor, begins before the rash appears, continues for several weeks in those without complications, but does not occur within the nervous system. In contrast, the effector phase of the immune response, as measured by the release of soluble CD8, coincides with the appearance and disappearance of the rash and occurs within the nervous system during encephalomyelitis.
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PMID:Immune activation in measles. 249 61

Infection of BALB/c mice with the M variant of encephalomyocarditis virus resulted in the development of a paralytic syndrome in 7 to 10 days. The paralysis was maximal during the period of viral clearance; most of the animals recovered from the initial deficit and showed no delayed recurrences. Pathologically, the white matter of brain and spinal cord showed well-demarcated areas of perivascular cuffing, demyelination, and, during recovery, remyelination by oligodendrocytes--all suggestive of postinfectious encephalomyelitis. Depletion of either the CD4 or CD8 subset of T cells in vivo with the appropriate monoclonal antibody, GK1.5 or 2.43, respectively, administered one day (24 h) prior to infection was sufficient to limit the development of the paralytic syndrome by 79% (GK1.5) and 82% (2.43).
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PMID:Treatment of encephalomyocarditis virus-induced central nervous system demyelination with monoclonal anti-T-cell antibodies. 255 Jun 66

Infection of athymic (nu/nu) mice with Theiler's murine encephalomyelitis virus results in an acute encephalitis which resembles poliomyelitis. Immunohistochemistry and in situ hybridization were used to delineate the presence of viral proteins and RNA in the nervous systems of nude mice infected with the Daniels strain of Theiler's virus. This system permits the analysis of a viral infection in the absence of an effective immune response. By immunohistochemistry, viral antigen was found in the processes and cell bodies of neurons and glial cells. Besides the presence of viral antigen in these cell types, by in situ hybridization, Theiler's virus RNA was also found in cells associated with vascular endothelium in the brains and spinal cords of these infected mice. Theiler's virus RNA-positive endothelial cells were observed not only near the primary lesions but also away from demonstrable lesions in normal-appearing regions in the central nervous system. Earlier work had suggested an intra-axonal dissemination for this virus (M. C. Dal Canto and H. L. Lipton, Am. J. Pathol. 106:20-29, 1982). Our findings are consistent with this model but also suggest an additional mechanism for virus spread within the central nervous system, i.e., by infecting vascular cells and crossing the blood-brain barrier. Lastly, after Theiler's murine encephalomyelitis virus infection, not only glial cells but also endothelial cells express major histocompatibility complex class II (la) antigen on their surface (M. Rodriguez, M. L. Pierce, and E. A. Howie, J. Immunol. 138:3438-3442, 1987). Our demonstration of Theiler's virus-infected endotheliumlike cells may explain interactions of virus products in stimulating antigen presentation.
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PMID:Theiler's virus infection in nude mice: viral RNA in vascular endothelial cells. 284 61

Infection of HeLa cells by poliovirus results in an abrupt inhibition of host cell protein synthesis. It is thought that the mechanism of this inhibition involves proteolytic cleavage of the p220 component of the cap-binding protein complex, thereby causing functional inactivation of the cap-binding protein complex and preventing capped (cellular) mRNAs from binding ribosomes. Current data suggest that the viral proteinase 2A indirectly induces p220 cleavage via alteration or activation of a second proteinase of cellular origin. We present evidence that translation of poliovirus proteinase 2A sequences in vitro activates p220 cleavage. We have also aligned published picornavirus 2A amino acid sequences for maximum homology, and we show that the picornaviruses can be divided into two classes based on the presence or absence of a highly conserved 18-amino acid sequence in the carboxy-terminal portion of 2A. This conserved 2A sequence is homologous with the active site of the cysteine proteinase 3C common to all picornaviruses. We show that picornaviruses which contain the putative 2A active site sequence (e.g., enteroviruses and rhinoviruses) will induce cleavage of p220 in vivo. Conversely, we show that two cardioviruses (encephalomyocarditis virus and Theiler's encephalomyelitis virus) do not encode this putative proteinase sequence in the 2A region and do not induce cleavage of p220 in vivo. The foot-and-mouth disease virus (FMDV) 2A sequence represents an apparent deletion and consists of only 16 amino acids, most homologous with the carboxy terminus of the cardiovirus 2A sequence. It does not contain the putative cysteine proteinase active site. However, FMDV infection induces complete cleavage of BK cell p220, and translation of FMDV RNA in vitro induces an activity that cleaves HeLa cell p220. The data predict that an alternate FMDV viral protease is responsible for the induction of p220 cleavage.
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PMID:Relationship of p220 cleavage during picornavirus infection to 2A proteinase sequencing. 284 33

Infection of the central nervous system by Theiler's murine encephalomyelitis virus (TMEV), a picornavirus, produces chronic demyelinating disease in susceptible mice. In this immunoelectron microscopic study of TMEV infection of neonatal mouse brain cells in culture, TMEV antigen was found on the surfaces of infected oligodendrocytes and astrocytes by labeling with hyperimmune serum from TMEV-infected mice or with rabbit antiserum to purified inactivated DA strain TMEV. Brain-derived macrophages had no TMEV-specific antigen on their surfaces and were not able to maintain productive TMEV infection, even though TMEV antigen was present in the cytoplasm. The presence of TMEV antigens on the surfaces of oligodendrocytes (myelin-producing cells) was unexpected because picornaviruses are nonenveloped viruses and do not bud from cell surfaces. The finding is consistent with the hypothesis that demyelination follows damage of infected oligodendrocytes by immune cells or immunoglobulins that recognize surface virus antigen.
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PMID:Theiler's virus-associated antigens on the surfaces of cultured glial cells. 284 58


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