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)

Numerous studies suggest that a viral infection, on the appropriate genetic background, may play an important pathogenetic role in the development of multiple sclerosis (MS). Among the several viral models of demyelination that have been investigated during the past two decades, Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease has emerged as one of the best because, similarly to MS, it is based on a combined viral-immune pathogenesis. This review highlights the following salient features of this model. TMEV-induced demyelinating disease is a chronic process, lasting for the life of the animals. Lesions consist of well-demarcated plaques of demyelination, which are strictly related to the presence of mononuclear cell infiltrates. Myelin degeneration is not due to direct viral cytopathic effects, but is rather dependent on the host immune response. Susceptibility/resistance to the disease is genetically regulated, and multiple genes both in and outside the major histocompatibility complex appear to be involved. The best immunological parameter that correlates with susceptibility is the ability of a murine strain to mount a delayed-type hypersensitivity (DTH) response to one or more viral epitopes. The importance of the DTH response against the virus in the pathogenesis of the disease is supported by the prevalent role of TH1 T-helper cells, known to be responsible for DTH responses, in inflamed CNS tissues. The role of DTH responses in the pathogenesis of demyelination is supported by the presence of numerous macrophages in affected CNS and by a direct relationship between the number of macrophages, their persistence in tissues, and the severity of lesions. Macrophages, in addition, are the main reservoir of the virus in the CNS, and their infectability correlates with susceptibility to the disease process. It is hypothesized that following the DTH response to the virus, activated lymphocytes recruit other inflammatory cells, particularly macrophages, into the infected CNS tissues. These nonspecifically recruited cells would secrete a number of proinflammatory molecules and proteases that would destroy myelin as a "bystander effect."
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PMID:Theiler's Murine Encephalomyelitis Virus (TMEV)-Induced Demyelination: A Model for Human Multiple Sclerosis 895 56

This report describes two mechanisms by which virus infection can facilitate demyelinating autoimmune inflammation in the murine CNS. In the BALB/c mouse model of experimental allergic encephalomyelitis (EAE), peripheral infection with an avirulent strain (A7) of Semliki Forest virus (SFV) increased the morbidity to EAE by infecting endothelial cells and damaging the blood-brain barrier (BBB). An influx of hematogenous CD18+ (LFA-1+ and MAC-1+) cells into the CNS compartment was followed by a local increase in intercellular adhesion molecule 1 (ICAM-1) expression on the vascular endothelium. Although SFV A7 infection without EAE induction caused multifocal cerebral vascular endothelial cell infection and BBB damage followed by cellular infiltration and transient increase of ICAM-1, inflammation and demyelination of CNS white matter with classical clinical signs of EAE was observed only in EAE-induced BALB/c mice, whereas the control mice remained neurologically healthy. The upregulation of ICAM-1 after virus infection was detected after the CD18+ (LFA-1+ and MAC-1+) cells had infiltrated the CNS both after EAE induction and also in nonsensitized control mice. The observed increase in ICAM-1 expression was transient in nonsensitized SFV A7 infected mice just as in the cellular infiltrates in the CNS, but EAE induction resulted in prolongation in both the cellular infiltrates and upregulation of ICAM-1. Thus, SFV A7 infection causes BBB damage and prolongs increased ICAM-1 expression on brain endothelium. This results in increased and more rapid morbidity to EAE in mice which have been sensitized with neuroantigen. However, SFV A7-infected mice without neuroantigen sensitization remain neurologically healthy.
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PMID:Blood-brain barrier breakdown and increased intercellular adhesion molecule (ICAM-1/CD54) expression after Semliki Forest (A7) virus infection facilitates the development of experimental allergic encephalomyelitis. 896 3

The DA strain of Theiler's murine encephalomyelitis virus, a member of the cardiovirus genus of picornaviruses, induces a restricted and persistent infection associated with a demyelinating process following intracerebral inoculation of mice; both virus infection and the immune response are believed to contribute to the late white matter disease. We now report that intraperitoneal inoculation with DA produces an acute myositis that progresses to a chronic inflammatory muscle disease in CD-1 mice as well as several inbred mouse strains. Some mouse strains also develop central nervous system white matter disease and a focal myocarditis. Infectious virus in skeletal muscle falls to undetectable levels 3 weeks postinoculation (p.i.), although viral genome persists for at least 12 weeks p.i., the longest period of observation. Severe combined immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting that DA virus is capable of inducing chronic muscle disease in the absence of an immune response. The presence in immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus suggests that the immune system also contributes to the pathology. T lymphocytes are the predominant cell type infiltrating the skeletal muscle during the chronic disease. This murine model may further our understanding of virus-induced chronic myositis and help to clarify the pathogenesis of human inflammatory myopathies.
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PMID:Theiler's murine encephalomyelitis virus-induced cardiac and skeletal muscle disease. 897 Oct 22

We compared infection of a murine macrophage-like cell line, J774-1, with two Theiler's murine encephalomyelitis virus subgroup strains. The GDVII strain, which is highly virulent and produces acute polioencephalomyelitis in mice, did not actively replicate in J774-1 cells, although there was a significant inhibition in cellular protein synthesis. In contrast, the DA strain, which is less virulent and causes demyelination with a persistent virus infection, productively infected J774-1 cells; however, there was less virus produced than in BHK-21 cells, and there was little if any cellular protein shutoff. These in vitro data may provide some explanation for the biological activities that are observed between both subgroup strains.
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PMID:Theiler's murine encephalomyelitis virus subgroup strain-specific infection in a murine macrophage-like cell line. 898 6

Experimental allergic encephalomyelitis (EAE) is facilitated in resistant BALB/c mice by intraperitoneal infection with an avirulent Semliki Forest virus (SFV-A7). Viral infection increases the incidence of EAE from 15-30% to 60-90% and speeds up appearance of paralysis from 24 to 14 days. In this paper, we describe treatment of virus-facilitated EAE with monoclonal antibodies (mAbs) against leukocyte and/or endothelial cell adhesion molecules. Therapy with mAb against ICAM-1 (intercellular adhesion molecule-1) had a modest effect, but caused hemorrhagic brain and spinal cord lesions. Therapy with mAb against Mac-1 (alpha M beta 2-integrin) was well tolerated but had no effect. Therapy with mAb against VLA-4 (alpha 4 beta 1-integrin) was safe, diminished both clinical and histopathological signs of EAE, decreased induction of VCAM-1 (vascular cell adhesion molecule-1) on brain vessels and diminished infiltration of VLA-4+ cells into the brain. The amount of viral antigen in the brain was not altered. We conclude that facilitation of leukocyte entry into the brain is a major mechanism for viral facilitation of EAE in the BALB/c mouse, and that facilitation can be inhibited by anti-adhesion therapy. This may have implications for treatment of relapses triggered by viral infections in multiple sclerosis.
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PMID:Therapy with antibody against leukocyte integrin VLA-4 (CD49d) is effective and safe in virus-facilitated experimental allergic encephalomyelitis. 900 49

The neurotropic mouse hepatitis virus MHV-JHM induces central nervous system (CNS) demyelination in Lewis rats that pathologically resembles CNS lesions in multiple sclerosis. The mechanisms of MHV-JHM-induced demyelination remain unclear and several studies have implicated the role of the immune response in this process. We have shown previously that protective immunity against MHV-JHM-induced encephalomyelitis was induced by immunization with a vaccinia virus (VV) recombinant expressing MHV-JHM S-protein (VV-S). Here, we present evidence that the time of MHV-JHM challenge after immunization with VV-S plays a critical role in protective immunity. The induction of virus-neutralizing S-protein-specific antibodies prior to the MHV-JHM challenge modulates the disease process and a subacute encephalomyelitis based on a persistent virus infection developed. Typical pathological alterations were lesions of inflammatory demyelination. In addition, the results indicate that after seroconversion, CD8+ T cells were no longer essential for virus elimination in contrast to their role in protection during acute encephalomyelitis.
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PMID:Coronavirus-induced encephalomyelitis: balance between protection and immune pathology depends on the immunization schedule with spike protein S. 904 33

Theiler's murine encephalomyelitis virus-induced immunologically mediated demyelinating disease (TMEV-IDD) in susceptible mice provides a relevant infectious model for multiple sclerosis. Previously, we have identified six major linear antibody epitopes on the viral capsid proteins. In this study, we utilized fusion proteins containing individual capsid proteins and synthetic peptides containing the linear antibody epitopes to determine the potential role of antibody response in the course of virus-induced demyelination. Preimmunization of susceptible mice with VPI and VP2 fusion proteins, but not VP3, resulted in the protection from subsequent development of TMEV-IDD. Mice free of clinical symptoms following preimmunizations with fusion proteins displayed high levels of antibodies to the capsid proteins corresponding to the immunogens. In contrast, the level of antibodies to a particular linear epitope, A1C (VP1(262-276)), capable of efficiently neutralizing virus in vitro increased with the progression of disease. Further immunization with synthetic peptides containing individual antibody epitopes indicated that antibodies to the epitopes are differentially effective in protecting from virus-induced demyelination. Taken together, these results suggest that antibodies to only certain linear epitopes are protective and such protection may be restricted during the early stages of viral infection.
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PMID:Major linear antibody epitopes and capsid proteins differentially induce protective immunity against Theiler's virus-induced demyelinating disease. 906 Jun 73

Several neurological complications associated with Influenza virus infection are known as a febrile convulsion, polyneuritis, meningitis, encephalomyelitis and encephalopathy. Influenza encephalopathy is the most severe complication associated with Influenza. It may be classified into several subtypes according to the clinical symptoms and laboratory data. In this review, Reye's syndrome, acute necrotizing encephalopathy and hemorrhagic shock and encephalopathy syndrome (HSE) are described in detail. The 1995 influenza pandemia in Nagasaki prefecture was markedly neurovirulent and lethal. Twelve cases developed influenza encephalopathy, and the mortality rate between them was 50%. Almost all of them had never be inoculated of influenza vaccine before.
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PMID:[Neurological outcome associated with influenza viral infection]. 910 88

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

Mice develop a fatal encephalomyelitis after infection with the Trinidad donkey strain of Venezuelan equine encephalitis (VEE) virus. Adult mice were inoculated intraperitoneally with VEE virus and the brains were examined at different time points. Morphological changes were assessed by histological staining. VEE virus antigen was detected with immunoperoxidase staining, and DNA fragmentation was evaluated in situ using the terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. VEE antigen was found in many areas of the brain and it was prominent in neurons. There were mild associated inflammatory changes. DNA fragmentation was demonstrated in many of these areas using TUNEL. In areas with TUNEL staining, morphological neuronal changes ranged from nuclear chromatin condensations to nuclear and cellular fragmentation, which are characteristic of apoptosis. There is strong morphological and biochemical evidence of apoptotic cell death in this experimental model of VEE virus infection.
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PMID:Apoptotic cell death is an important cause of neuronal injury in experimental Venezuelan equine encephalitis virus infection of mice. 911


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