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Query: UMLS:C0014070 (encephalomyelitis)
13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of HLA-A, B, DR antigens was studied in 24 patients with acute measles encephalomyelitis compared to 1926 control subjects. The results demonstrated no association between the susceptibility to the disease and HLA markers. However, DR4 was observed in 6 patients out of 10 who developed intrathecal secretion of specific antimeasles immunoglobulins, while absent in 4 patients, who did not (p less than 0.04). Further studies on a larger series are needed.
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PMID:HLA antigens in acute measles encephalitis. 348 99

Lewis and Brown Norway (BN) rats which are susceptible or resistant to autoimmune reactions against brain antigen, respectively, were inoculated intracerebrally with a neurotropic measles virus. Suckling rats died from a rapidly fatal acute encephalopathy (AE). With increasing age Lewis rats developed a subacute measles encephalomyelitis (SAME) whereas BN rats showed a clinically silent encephalitis (CSE). Infectious virus could occasionally be recovered from SAME animals using cocultivation techniques but not from BN rats with CSE. With monoclonal antibodies against measles virus, viral proteins were localized in brain tissue. Nucleocapsid and phosphoprotein were detected in infected brain cells of all animals with AE, SAME and CSE, whereas measles virus haemagglutinin, fusion and matrix proteins were either reduced or absent, suggesting a restricted synthesis of measles virus envelope proteins. These data suggest that the different diseases of the two rat strains are related to the immunogenetic background rather than to the replication of measles virus in the central nervous system. This animal model provides the opportunity to investigate further the events occurring during establishment of measles virus persistence in the brain, and the genetic control of associated immunological and immunopathological reactions.
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PMID:Virological aspects of measles virus-induced encephalomyelitis in Lewis and BN rats. 349 33

An experimental central nervous system (CNS) disease that bears some similarity to human multiple sclerosis and that is associated with infection by measles virus has been induced in hamsters. This disease has been described previously (Carrigan and Johnson: Proceedings of the National Academy of Sciences 77:4297-4300, 1980). At that time, it was believed that the disease was restricted to the spinal cords of affected animals. The present work demonstrates that the disease can also affect the brain, describes in more complete detail the types of clinical disease that occur, illustrates the histopathological changes found in diseased CNS tissues, and documents more accurately the incidence of the disease in the virally infected animals. In summary, the disease, which has now been termed chronic, relapsing encephalomyelitis (CRE) is associated with neonatal CNS infection of hamsters with a particular strain of measles virus. CRE occurs in approximately 12% of animals that survive the acute viral infection, and of these affected animals about half develop detectable clinical signs of neurological disease. The balance of the animals have subclinical disease detectable only by histopathologic changes within the CNS. These lesions are composed of varying degrees of demyelination, necrosis, mononuclear cell inflammation, and gliosis.
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PMID:Chronic, relapsing encephalomyelitis associated with experimental measles virus infection. 355 27

We studied 19 patients with postinfectious encephalomyelitis complicating natural measles-virus infections, and our results support the hypothesis that this demyelinating disease has a pathogenesis similar to that of experimental allergic encephalomyelitis. Early myelin destruction was demonstrated by the presence of myelin basic protein in cerebrospinal fluid, and lymphocyte proliferative responses to myelin basic protein were found in 8 of 17 patients tested. A lack of intrathecal synthesis of antibody against measles virus suggests that measles encephalomyelitis may not be dependent on virus replication within the central nervous system. Similar lymphoproliferative responses to myelin basic protein of lymphocytes from single patients with encephalomyelitis after rabies vaccine or after varicella or rubella virus infections suggest a common immune-mediated pathogenesis for the perivenular demyelinating disease that can follow the injection of neural tissues or infection by a variety of viruses.
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PMID:Measles encephalomyelitis--clinical and immunologic studies. 619 51

Measles encephalomyelitis appears to be an immune-mediated parainfectious disorder, but it is unclear whether viral invasion of brain is an obligate step in its development. Immunocytochemical methods were used to search for virus antigen in formalin-fixed, paraffin-embedded central nervous system (CNS) tissues from 10 patients with measles encephalomyelitis and 12 patients who had died of measles without CNS involvement. All the CNS tissues studied were viral antigen negative. Similarly fixed CNS tissues from all of 6 patients with subacute sclerosing panencephalitis were viral antigen positive and served as controls. The pattern of perivenular demyelination was also determined in 4 cases of measles encephalomyelitis using antibodies to myelin associated glycoprotein and myelin basic protein and a Luxol fast blue stain. Areas of demyelination in serial sections were quantitated, and no morphometrical differences were found among tissues stained with the three stains. The data suggest the lack of virus replication in the CNS during encephalomyelitis or fatal measles without CNS symptoms. The pattern of loss of myelin associated glycoprotein and myelin basic protein in regions of perivenular demyelination resembles that reported in experimental allergic encephalomyelitis. This pattern of demyelination has been proposed to result from a primary attack on the myelin sheath rather than from direct involvement of the oligodendroglial cell.
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PMID:Measles encephalomyelitis: lack of evidence of viral invasion of the central nervous system and quantitative study of the nature of demyelination. 620 79

The blast transformation test revealed a high level of lymphocyte sensitization to human acute encephalomyelitis virus in 12 out of 29 (41.9%) patients with multiple sclerosis in the early stages of the disease and in the period of exacerbation in patients with long-term disease. The pattern of the blast transformation test in response to herpes simplex and measles viruses did not depend on the duration of the disease. High, moderate, and low levels of lymphocyte blast transformation reaction to herpes and measles viruses were observed in patients with multiple sclerosis with similar average durations of the disease.
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PMID:[Cellular immunity study of multiple sclerosis in the lymphocyte blast transformation reaction to the viruses of acute human encephalomyelitis, herpes and measles]. 629 70

Serological examinations of blood sera from patients with multiple sclerosis (MS), their nearest relatives, and subjects of the control groups for antibodies to causative agents of some viral infections demonstrated antihemagglutinins to measles and rubella viruses in 61%-95.5% of the subjects examined in all the groups, to mumps virus in 53% in MS patients, to tick-borne encephalitis virus in 2.2% in the same group, and in 10.5% in the group of patients with other CNS diseases, and none in healthy subjects. Virus-neutralizing antibodies to human acute encephalomyelitis virus (HAEM) in 28% of the cases, frequently in the stage of remission. Specific IgM to measles virus was found in 41% of MS patients, in 15% of their nearest relatives, and in 19.7% of patients with other CNS diseases, but not in healthy subjects. No differences in the rate of antibody findings to herpes simplex virus types 1 and 2 were observed in the groups examined. The rate of detection of virus-neutralizing antibody to HAEM virus was significantly higher in MS patients with the severity of the course of IV-V degree (20%) than of the II-III degree (8.8%). In the period of MS exacerbation the level of specific IgM to measles virus increased (35.6%), and higher titres of antihemagglutinins were observed in patients with longer duration of the disease and higher degree of its severity.
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PMID:[Detection of antibodies to the causative agents of viral infections in multiple sclerosis patients]. 684 21

Autoreactive T cells specific for myelin basic protein (MBP), a major component of central nervous system (CNS) protein, are frequently found in blood and cerebrospinal fluid of patients with postinfectious encephalomyelitis. This autoimmune syndrome is a CNS complication after infections with a number of different enveloped viruses, e.g. mumps, measles, rubella, influenza and varicella. However, the pathophysiological mechanism leading to this breaking of natural self tolerance in the course of viral infection remains an enigma. A long-lasting hypothesis has suggested that incorporation of cellular (self) proteins into the envelope of budding viruses might be a possible mechanism leading to autosensitization. In a model study we demonstrate here that vesicular stomatitis virus (VSV), grown in myelin protein-expressing cell cultures, is highly efficient in triggering T cell responses to MBP in vitro and can prime autoreactive T cell immune responses in vivo. On the basis of these findings, we suggest that incorporation of CNS membrane components into the viral envelope and subsequent priming of self-reactive immune responses might be the common pathogenic mechanism underlying the postinfectious encephalomyelitis syndrome.
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PMID:Autoimmunity caused by host cell protein-containing viruses. 753 Dec 73

Neurologic diseases are important complications of measles. The role of virus infection of the central nervous system as well as the route of virus entry has been unclear. Five autopsied cases of individuals who died with severe acute measles 3-10 d after the onset of the rash were studied for evidence of viral involvement of the central nervous system. In all cases, in situ hybridization and RT-PCR in situ hybridization techniques showed endothelial cell infection. Immunoperoxidase staining with an anti-ferritin antibody revealed a reactive microgliosis. These data suggest that endothelial cells in the brain are frequently infected during acute fatal measles. This site of infection may provide a portal of entry for virus in individuals who subsequently develop subacute sclerosing panencephalitis or measles inclusion body encephalitis and a target for immunologic reactions in post-measles encephalomyelitis.
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PMID:Brain endothelial cell infection in children with acute fatal measles. 759 37

Secondary vaccine failure (SVF) of measles is generally believed to run a milder course of illness than an ordinary course of infection. Severe complications such as central nervous system involvement have rarely been reported. A 12 year old girl, who had received a live attenuated measles vaccine 10 years earlier, developed an encephalomyelitis in the absence of symptoms indicative of ordinary measles such as Koplik spots. Anti-measles hemagglutination inhibition (HI) titer and measles IgM and IgG antibody titers were measured in a commercial laboratory. Measles virus genomic sequence was detected by polymerase chain reaction. Both serum and cerebrospinal fluid (CSF) samples obtained at acute phase already showed extremely high titers of HI (x8192 in serum and x1024 in CSF, respectively) and IgG antibody along with the presence of IgM antibody. Polymerase chain reaction detected the measles virus genomic sequence in the acute phase CSF. The patient's definite history of measles vaccination, high titers of HI and IgG antibodies observed at the very early stage of illness and the clinical course indicated that this patient has an encephalomyelitis due to SVF of measles. It is suggested that measles virus can be a pathogen of encephalitis without symptoms indicative of ordinary measles in individuals who received live attenuated measles vaccines.
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PMID:Measles encephalomyelitis in a patient with a history of vaccination. 764 92


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