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)

The questions how a viral infection induces cellular autoimmune reactions (CMAI) and which components of both virus and auto-antigen play part in this process were addressed in our animal model of measles virus (MV)-induced CMAI against myelin basic protein (MBP) during subacute measles encephalitis (SAME). In an attempt to define whether cellular or humoral immune responses are involved in the occurrence of the autoimmune based disease process, Lewis rats were treated with different combinations of antibodies and T cells reactive with either MV and its structural proteins or MBP and MBP-peptides. The only treatment combination after which experimental allergic encephalomyelitis (EAE)-like disease and pathology developed was when non-encephalitogenic T cells reactive against residues 69-81 of MBP were adoptively transferred into MV-infected Lewis rats. The results of the study show that T cells which are non-encephalitogenic in the normal central nervous tissue are capable of inducing an allergic encephalomyelitis in animals with a viral infection involving the brain.
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PMID:Synergistic interaction between measles virus infection and myelin basic protein peptide-specific T cells in the induction of experimental allergic encephalomyelitis in Lewis rats. 768 89

The characteristic disease features of measles--fever and rash--are associated with the immune response to infection and are coincident with virus clearance. MV-specific antibody and CD4 and CD8 T cell responses are generated and contribute to virus clearance and protection from reinfection. During this same phase of immune activation immunologic abnormalities are also apparent. There is a generalized suppression of cellular immune responses that may contribute to increased susceptibility to other infections. Autoimmune disease may appear in the form of acute disseminated encephalomyelitis. If virus-specific immune responses are inadequate infection may progress with pulmonary or CNS manifestations, but without a rash. The pathogenesis of the rare disease SSPE, that occurs many years after primary infection is not clear, but immune responses show increased antibody to measles and cellular immune responses similar to those seen after uncomplicated infection.
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PMID:Immune responses during measles virus infection. 778 55

Canine distemper (CD) is a frequently fatal, systemic morbillivirus infection in the dog and other carnivores: encephalomyelitis is the common cause of death. Susceptibility to canine distemper virus (CDV) is now recognized in a wide range of non-domestic animals, most recently in captive lions, tigers and leopards. Furthermore, closely related viruses have produced CD-like diseases in marine mammals. CDV induces an inclusion-body encephalomyelitis in the dog and demyelination is often a conspicuous feature. Myelin injury is associated with the presence of virus but the mechanism of demyelination remains incompletely understood. Oligodendrocyte infection may be defective, as has been shown in vitro. CDV and measles virus (MV) produce similar systemic disorders in their respective hosts but differ markedly in the frequency of central nervous system (CNS) involvement, and in the pathogenesis of the more common neurological sequelae. Both CDV and MV have been considered as multiple sclerosis agents, and the association of CDV with other human disease has been suggested.
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PMID:Aspects of canine distemper virus and measles virus encephalomyelitis. 789 14

Measles virus causes a severe systemic illness. The rash occurs simultaneously with the onset of the effector phase of the antiviral immune response and substantial evidence of immune activation. This immune response is effective in clearing virus and in establishing long-term resistance to reinfection but is associated with immune suppression, autoimmune encephalomyelitis, and increased susceptibility to secondary infections. This apparent paradox may be explained in part by preferential long-term activation of type 2 CD4+ T cells by measles virus infection. Preferential stimulation of type 1 CD4+ T cells by inactivated virus vaccines is hypothesized to play a role in subsequent development of atypical measles.
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PMID:Pathogenesis of measles virus infection: an hypothesis for altered immune responses. 793 Jul 50

Recovery from viral infection is a result of very complex interactions between specific and nonspecific immune reactions and the infectious agent. A variety of immune mechanisms are undoubtedly important factors in this event and operate together in overcoming the infectious process. However, despite much available information about these viral defense mechanisms, it has proved remarkably difficult to assign a determinative role in vivo to any single antiviral immunological mechanism in recovery from a single viral disease, particularly since the immune response to the virus itself may frequently contribute to the pathology of the disease. Furthermore, if virus-induced immune responses are also directed against normal host components, this may set the stage for an autoimmune disease. In this context acute measles encephalomyelitis is of interest since in this disease autoimmune reactions against brain antigens have been observed and considered of pathogenetic importance. In this short review, virological and immunological findings of measles virus infections in a rat model in relation to autoimmune reactions will be presented and the mechanisms by which measles virus may alter host reactivity against self-antigens discussed.
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PMID:Measles virus-induced autoimmune reactions against brain antigen. 840 53

Nine patients below 20 years of age (4 males and 5 females), who were diagnosed to have acute disseminated encephalomyelitis (ADEM) by clinical findings and magnetic resonance imaging (MRI), were reviewed retrospectively. They ranged from 4 months to 20 years of age with an average of 8.6 years. Seven patients (78%) received neurophysiological studies, which included electroencephalography, multimodality evoked potentials (EPs), nerve conduction velocity and/or F-wave measurement. The presentation symptoms were mainly headache, vomiting, consciousness change and motor deficits. Seven (78%) of nine patients had symptoms preceded by fever or upper respiratory tract infections; one (11%) was preceded by trivalent mumps, measles, rubella vaccination and no definite predisposing factor was found in another. Computed tomography (CT) scans were abnormal in five (71 %) of seven children, while MRI showed multiple lesions in seven (78%) of nine children. The lesions in MRI were mainly in the brainstem (n = 6), basal ganglion (n = 5), thalamus (n = 4), periventricular white matter (n = 4) and cerebellum (n = 4). EPs disclosed spinal cord involvement in all patients who received the examination. Peripheral neuropathy was disclosed in one patient. It was concluded that associated radiculoneuropathy is possible in patients with ADEM. Both MRI and neurophysiologic studies are complementary for diagnosis of ADEM.
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PMID:Acute disseminated encephalomyelitis in children: clinical, neuroimaging and neurophysiologic studies. 875 75

Acute disseminated encephalomyelitis (ADEM) occurs late in the course of viral infection, mainly exanthematous diseases such as measles, chicken pox, and rubella. Postinfectious encephalomyelitis is characterized by immune-mediated demyelination, which is found in experimental autoimmune encephalomyelitis (EAE), and virus cannot be isolated from the central nervous system. The investigations using animal models infected with. Theiler's virus or measles virus would be very useful for clarifying the mechanisms of demyelination induced by viral infection. Although the incidence of postvaccinal encephalomyelitis has fallen markedly due to development of vaccines, the neurological complications following immunization are still reported. The vaccines prepared from viruses other than live-attenuated viruses and whole-killed organisms have never been proved to induce ADEM.
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PMID:[Acute disseminated encephalomyelitis]. 910 97

Acute measles is a classic infectious disease of childhood with worldwide distribution. Its causative agent, measles virus (MV), is an efficient pathogen, persisting in nature in populations large enough to support it, even though it is able to cause an acute infection in any individual only once in his lifetime. The characteristic clinical hallmarks of measles, fever and rash, coincide with antiviral immune response. MV-specific T lymphocyte and antibody responses contribute to virus clearance and protection from reinfection, respectively. Concomitant with immune activation immunologic abnormalities arise during MV infection. The ensuing suppression of cellular immune responses is presumably responsible for increased susceptibility to other infections. Additionally, central nervous system (CNS) complications of MV infection with different pathogenesis occur. Autoimmune disease may appear in the form of acute measles encephalomyelitis. Furthermore, MV may persist in the CNS in rare cases without periodic shedding of infectious virus. Measles inclusion body encephalitis can develop on the basis of inadequate virus-specific cell-mediated immune responses and subacute sclerosing panencephalitis occurs many years after primary measles as a slow virus infection. Host cell factors operating in cells of the CNS together with mutations particularly in genes coding for viral envelope proteins initiate and maintain the persistent state of infection with a viral replication cycle that is attenuated at the transcriptional and translational level.
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PMID:Measles virus infections of the central nervous system. 945 Feb 34

Some autoimmune complications such as postinfectious encephalomyelitis are associated with immunologic abnormalities induced by measles virus infection. To address the superantigenic stimulation in measles which might be related with autoimmune complications, T-cells bearing the TCRBV5S2 or TCRBV8 chains and the expression of activation markers were analyzed by monoclonal antibodies. To estimate clonal expansions, the CDR3 length profile in T-cells bearing the TCRBV5S2 or TCRBV8 chains was analyzed by two-stage PCR. Results showed that the expression of DR molecules in CD3+ cells was increased significantly in measles patients (19.6 +/- 20.7%) compared to healthy children (2.9 +/- 1.4%). The mean percentage (7.1 +/- 4.4%) of T-cells bearing the TCRBV8 chain was increased in measles patients compared to healthy children (5.6 +/- 3.1%). The percentage of T-cells bearing the TCRBV5S2 chain in measles patients (3.0 +/- 1.2%) was similar to that in healthy children (2.7 +/- 0.6%). By analysis of the CDR3 length we found that there was no evidence of clonal expansions in T-cells bearing the TCRBV8 chain and that there were clonal expansions in T-cells bearing the TCRBV5S2 chain. These data suggest a conventional antigenic stimulation with T-cells bearing the TCRBV5S2 chain and a superantigenic stimulation with T-cells bearing the TCRBV8 chain may occur in the acute stage of measles infection.
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PMID:Clonal expansion of T-cells in measles. 984 Jun 83

The patient is a 10-year-old male who experienced somnolence and incomplete quadriplegia after headache and vomiting, without exanthema, for 3 days. The clinical course and magnetic resonance imaging findings of the brain and spinal cord were compatible with acute disseminated encephalomyelitis. The serologic examination revealed that the patient had rubeola because titers of IgM and IgG antibody to measles virus measured by enzyme immunoassay were 0.91 and 40 (cutoff = 0.80 and 2), respectively, at 5 weeks after the onset, the IgM titer had become negative (0.56), and the IgG titer had decreased to 17.7 at 13 weeks after the onset. Because the patient had received a measles-mumps-rubella vaccine at 12 months of age, the acute disseminated encephalomyelitis was thought to be attributed to the modified measles resulting from measles vaccine failure.
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PMID:Acute disseminated encephalomyelitis with probable measles vaccine failure. 1037 90


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