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)

After intracranial replication of a neurotropic strain of vaccinia in mouse brain, analysis of the purified virus preparation reveals the presence of at least one host protein on the virus which was identified as the myelin basic protein. Vaccinia virus Elstree, a dermotropic virus may substitute for complete Freund's adjuvant (CFA) in inducing experimental allergic encephalomyelitis (EAE). Guinea pigs challenged with virus-myelin emulsions without CFA developed clinical and histological signs of EAE.
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PMID:Mechanisms in the pathogenesis of post-infectious vaccinia virus encephalomyelitis in the mouse. 9 31

The effect of X-irradiation on experimental vaccinia infection of BALB/c mice was studied. As compared with nonirradiated controls, the X-irradiated animals exhibited (i) a time lag in virus replication (delayed, but protracted replication); (ii) a delayed and repressed immune response: (iii) more severe acute cytocidal infection of leptomeninges, choroid plexus, ependyma, and vessels, with extensive damage to the brain-barrier system; and (iv) noncytocidal, latent infection of glial cells and neurons. Several animals developed acute or subacute demyelination disease, resembling experimental allergic encephalomyelitis or postinfectious encephalomyelitis.
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PMID:Vaccinia virus infection of the central nervous system in X-irradiated mice. 50 Jan 84

Infection of mice with the JHM strain of mouse hepatitis virus (MHV) results in an acute encephalomyelitis associated with primary demyelination of the central nervous system. Efforts at understanding the components of the immune response in the development of chronic MHV-induced demyelination have implicated the antibody response and both the CD4+ and CD8+ T cell responses. In this report, we demonstrate that Balb/c (H-2d) mice immunized with the JHM (JHMV) strain of MHV develop a CD8+ cytotoxic T lymphocyte (CTL) response. One population of these virus-specific CTL recognize the nucleocapsid (N) protein. Recombinant vaccinia viruses expressing either the entire N protein or carboxy-terminal deletions were used to determine the number and location of the epitope(s) recognized. The CTLs were found to recognize a peptide contained within the carboxy-terminal 149 amino acids of the N protein. Analysis of infected cell lines expressing transfected major histocompatibility genes demonstrated that the anti-N protein CTLs were restricted exclusively to the Ld molecule. These data provide the first definition of a MHV-specific CTL response directed to a viral protein and suggest that the anti-N protein CTL response is one potential mechanism used by the host to clear JHMV from the central nervous system.
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PMID:Mouse hepatitis virus nucleocapsid protein-specific cytotoxic T lymphocytes are Ld restricted and specific for the carboxy terminus. 137 38

The effects of Neurotropin, a substance extracted from the inflammatory dermis of rabbits inoculated with Vaccinia virus, for experimental allergic encephalomyelitis (EAE) in Lewis rats, a model for human multiple sclerosis (MS), was studied. The peptide defined by residues 68-84 (MB 68-84) which corresponds to the encephalitogenic portion of the guinea pig myelin basic protein (MBP) in complete adjuvant H37Ra (CFA) was injected into the hind foot pad of each rat. Neurotropin significantly suppressed the clinical and histological expression of actively induced EAE when administered i.p. daily from day 0 to day 6 after immunization. In addition, passive EAE induced by precultured spleen cells from rats immunized with MB 68-84 in CFA was also suppressed by daily administration of Neurotropin after cell transfer. Neurotropin treatment significantly suppressed the delayed-type hypersensitivity (DTH) response to MB 68-84. Furthermore, the ability of spleen cells from Neurotropin-treated rats to transfer EAE was significantly lower than that of saline-treated rats. It seemed that the suppression may be due to the inhibition of the activation by MB 68-84 of sensitized spleen cells, as demonstrated by proliferative response to MB 68-84. However, no difference was observed in Con A-induced proliferative response of the spleen cells between Neurotropin- and saline-treated rats. These findings indicate that Neurotropin inhibits EAE by suppressing the immune responses to encephalitogenic MBP with little non-specific suppression.
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PMID:Neurotropin inhibits experimental allergic encephalomyelitis (EAE) in Lewis rats. 171 61

A hybrid vaccinia virus expressing a chimeric protein consisting of thymidine kinase and the encephalitogenic determinant, S1, from guinea pig myelin basic protein was constructed. Infection of guinea pigs with the virus resulted in the development of allergic encephalomyelitis.
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PMID:Viral chimeric protein including a determinant of myelin basic protein is capable of inducing allergic encephalomyelitis in guinea pigs. 172 19

The effect of neurotropin, an extract isolated from the inflamed skin of rabbits inoculated with Vaccinia virus was examined on acute experimental allergic encephalomyelitis (EAE) in Lewis rats. A dose of 40 mg per kg body weight of neurotropin was administered intraperitoneally for 7 days post-inoculation. The severity of clinical signs of acute EAE was decreased by the administration of neurotropin. Histopathologic evaluation showed that lesion severity of EAE in neurotropin-treated rats was less than that seen in untreated rats. Blood lymphocyte subset analysis revealed that in comparison to untreated EAE rats, in neurotropin-treated rats, the percentage of OX6+ (Ia antigen) cells was lower and the W3/25+ (helper T cell): OX8+ (suppressor/cytotoxic T cell) cell ratio was greater during the period of peak inflammation. Immunohistochemical examination of neurotropin-treated rats demonstrated that OX6+ and W3/25+ cells within EAE lesions were fewer and that OX8+ cells in lesions occurred in greater numbers than those in untreated rats. These findings suggest that the OX8+ cells in the inflammatory lesions may have been induced by neurotropin treatment and that the suppressive effects on the disease may have been causally related to their presence.
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PMID:Suppression of acute experimental allergic encephalomyelitis by neurotropin: clinical, histopathologic, immunologic and immunohistochemical studies. 195 67

The susceptibility of the C6/36 clone of Aedes albopictus monolayer cell cultures was determined with 46 prototype viruses passed through three subcultures. Viral growth was confirmed by titration of the passage material in other susceptible host systems. Nineteen viruses demonstrated good growth in C6/36 cells: coxsackievirus group A type 10 and group B types 2, 3, 4, and 5; enterovirus 69; mumps virus; poliovirus types 1 to 3; reovirus types 1 to 3; vaccinia virus; dengue virus type 2; eastern equine encephalomyelitis virus; La Crosse virus; Rocio virus; and St. Louis encephalitis virus. Ten viruses did not adapt to growth in the C6/36 cultures. Seventeen other virus strains displayed only limited growth which was primarily restricted to the initial C6/36 passage or was detected by hemagglutinin reactions without observable cell degeneration. Of the 46 viruses, 33 (72%) were capable of initiating infection with a demonstrable cytopathic effect in the initial C6/36 passage. Hemagglutination or complement fixation titers or both were obtained with dengue virus type 2, eastern equine encephalomyelitis virus, La Crosse virus, mumps virus, reovirus types 1 to 3, and Rocio, St. Louis encephalitis, and vaccinia viruses.
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PMID:Susceptibility of Aedes albopictus C6/36 cells to viral infection. 361 15

Results of virological examination of 239 samples taken from 84 children with neurological complications after smallpox vaccination are described. In postvaccinal encephalitis, vaccinia virus was isolated from blood, cerebrospinal fluid and pharyngeal secretions of 23 out of 40 children (57.5%) as well as from autopsy specimens sampled between 10-35 days after vaccination. During the acute period of disease, virus was detected in 17 out of 31 (54.2%) cerebrospinal fluid specimens. In 3 postvaccinal encephalitis cases the virus was present in brain and in a case of encephalomyelitis--in the spinal cord. These results confirmed the participation of vaccinia virus in the pathogenesis of postvaccinal encephalitis. The pathogenicity of vaccinia virus may be manifested only under a changed reactivity of the vaccinated host.
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PMID:Vaccinia virus in postvaccinal encephalitis. 613 34

If rabbits were given total body irradiation and infected wih vaccinia virus (strain Elstree) a severe disease developed with a viraemia lasting up to 12 days. The clearance of the virus from the peripheral blood was severely impaired by x-ray doses above 800 R. The attenuated vaccinia virus strain MV did not turn virulent, if it was injected to irradiated rabbits. With caution it can be assumed that live vaccines, containing attenuated viruses, may be given to immunosuppressed persons. Rats are not susceptible to ectromelia-virus (mouse-poxvirus); overt clinical sympatoms, however, with a mortality of 30 per cent developed in irradiated rats. This proofs that specific poxviruses can be transferred to another species. As the experimental conditions are unnatural, this may occur only rarely in immunosuppressed persons. After intracerebral infection of Balb-C-mice with low doses of vaccinia virus two types of infection were seen: 1. a severe cytocidal infection of leptomeninges, chorioid plexus and vessels; 2. a noncytocidal, latent infection of glial cells and neurons. Several animals developed a picture resembling experimental allergic encephalomyelitis. It seems that irradiation altered the antigenic conditions of the cytoplasmic membranes in non-cytocidally infected cells. The model might explain some processes in the pathogenesis of demylinating diseases.
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PMID:Studies on poxvirus infections in irradiated animals. 625 May 14

Viral infections have been associated with the initiation and exacerbations often observed with autoimmune disease. Mechanisms by which viruses may play a role in the development of autoreactive immune responses include polyclonal activation of B and T cells, molecular mimicry, viral infection of immune cells, exposure of sequestered antigens, or altered host cell expression (neoantigen or altered self) in virus infected host cells. We have been studying the immune response generated to self proteins in association with viral infection. Here we evaluate the effects of viral infection on the development of an autoimmune disease of the central nervous system, experimental allergic encephalomyelitis. A vaccinia virus construct, VVplp was made containing the coding region for rat myelin proteolipid protein (PLP). Cells infected with VVplp were found to express PLP protein in vitro. Central nervous system disease was not detectable in mice vaccinated with VVplp. However, mice vaccinated with VVplp and later challenged with encephalitogenic peptides derived from PLP were found to have enhanced disease with earlier onset of symptoms when compared to mice treated with a control vaccinia virus construct. This enhancement of disease was found to peak at 10 days post challenge with the encephalitogenic PLP peptide. Clinical disease and an inflammatory response in the central nervous system was evident in mice previously vaccinated with VVplp but not in control vaccinated mice at this time. These results indicate that prior infection with a virus capable of coding for self protein can predispose the host to an accentuated autoimmune response.
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PMID:Enhancement of autoimmune disease using recombinant vaccinia virus encoding myelin proteolipid protein. 769 50


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