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)

Human rabies is a fatal encephalomyelitis. After the development of the central nervous system infection, there is centrifugal spread of the rabies virus to extraneural (systemic) organs. With histochemical staining and localization of rabies virus antigen (RVA) with immunoperoxidase staining, we have examined tissue sections of organs from 14 postmortem pediatric and adult cases of human rabies acquired in Mexico and the People's Republic of China. RVA was found in nerve plexuses in multiple organs, including the gastrointestinal tract. RVA was observed in muscle fibers of the heart, tongue, and larynx. RVA frequently was observed in the adrenal medulla with an associated inflammatory reaction. Minor salivary glands of the tongue contained RVA and major salivary glands showed RVA in plexuses, but not in either acini or ducts. Epithelial cells of the tongue and taste buds were occasionally infected. RVA was observed in hair follicles of the skin and rarely in pancreatic islets. The infection of extraneural organs was sometimes, but not always, associated with an inflammatory reaction. These findings indicate that centrifugal spread of rabies virus to extraneural organs occurs frequently in human rabies.
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PMID:Extraneural organ involvement in human rabies. 1046 32

GDVII subgroup strains of Theiler's murine encephalomyelitis virus (TMEV) are highly virulent and produce acute polioencephalomyelitis in mice. Neither viral persistence nor demyelination is demonstrated in the few surviving mice. In contrast, DA subgroup strains are less virulent and establish a persistent central nervous system infection which results in demyelinating disease. We previously reported a subgroup-specific infection in a macrophage-like cell line, J774-1 cells; i.e., GDVII strain does not replicate in J774-1 cells, whereas the DA strain actively replicates in these cells. In addition, this subgroup-specific virus growth is shown to be related to the presence of L* protein, a 17 kDa protein translated out-of-frame of the viral polyprotein from an AUG located 13 nucleotides downstream from the polyprotein's AUG. The present paper demonstrated that this subgroup-specific infection is observed in murine monocyte/macrophage lineage cell lines, but not in other murine cell lines including neural cells. An RNase protection assay also suggested that L* protein-related virus growth is regulated at the step of viral RNA replication. As macrophages are reported to be the major cell harboring virus during the chronic demyelinating stage, the activity of L* protein with respect to virus growth in macrophages may be a key factor in clarifying the mechanism(s) of TMEV persistence, which is probably a trigger to spinal cord demyelination.
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PMID:Theiler's murine encephalomyelitis virus (TMEV) subgroup strain-specific infection in neural and non-neural cell lines. 1055 81

Treatment of nervous system Lyme disease depends on the severity and site of involvement. Although some data indicate that uncomplicated Lyme meningitis can be treated effectively with oral doxycycline, central nervous system infection (meningitis, radiculitis, encephalomyelitis, and cranial neuritis) is usually treated with parenteral antibiotics for 14 to 30 days, depending on disease severity, as is severe and progressive peripheral nervous system involvement. Ceftriaxone, 2 g/d, is the most commonly used regimen; cefotaxime, 2 g every 8 hours, appears to be equally effective. Penicillin in meningeal doses is also effective, perhaps slightly less so than the third-generation cephalosporins, but it is less convenient to administer. For patients with prohibitive drug allergies, treatment with oral doxycycline in doses of 300 to 400 mg/d may be effective. In patients with facial palsy or with indolent peripheral neuropathies, a trial of oral medication (doxycycline, 100 mg two or three times a day, or amoxicillin, 500 to 1000 mg three times a day for 21 to 30 days) is reasonable. Patients for whom this fails are treated with parenteral medications.
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PMID:Neuroborreliosis (Nervous System Lyme Disease). 1109 3

Theiler's murine encephalomyelitis virus (TMEV) infection is maintained in mouse colonies by fecal-oral spread (with no apparent role for persistent central nervous system infection) from an acutely infected animal to another. Therefore, serological methods offer the principal way to assess infection in mice and related rodent populations. Infection of mouse colonies with TMEV appears to be worldwide, yet no systematic serologic studies have been reported. In this study, enzyme-linked immunoassay and neutralization analysis of sera from feral Mus musculus obtained from four locations in the United States and one in Russia revealed antibodies to purified TMEV and two linear viral peptide epitopes in more than 50% of the sera derived from the five different locations. A similar analysis of sera from 26 species of related rodents trapped at multiple locations in North America and Europe indicated the presence of anti-TMEV antibodies only in a small proportion of water and bank voles that belong to a different subfamily. These results indicate that Mus musculus is the natural host of TMEV.
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PMID:Serological evidence that Mus musculus is the natural host of Theiler's murine encephalomyelitis virus. 1137 48

Theiler's murine encephalomyelitis viruses (TMEV) consist of two groups, the high- and low-neurovirulence groups, based on lethality in intracerebrally inoculated mice. Low-neurovirulence TMEV result in a persistent central nervous system infection in mice, leading to an inflammatory demyelinating pathology and disease. Low- but not high-neurovirulence strains use sialic acid as an attachment factor. The recent resolution of the crystal structure of the low-neurovirulence DA virus in complex with the sialic acid mimic sialyllactose demonstrated that four capsid residues make contact with sialic acid through noncovalent hydrogen bonds. To systematically test the importance of these sialic acid-binding residues in viral entry and infection, we mutated three VP2 puff B amino acids proposed to make contact with sialic acid and analyzed the consequences of each amino acid substitution on viral entry and spread. The fourth residue is in the VP3-VP1 cleavage dipeptide and could not be mutated. Our data suggest that residues Q2161 and G2174 are directly involved in BeAn virus attachment to sialic acid and that substitutions of these two residues result in the loss of or reduced viral binding and hemagglutination and in the inability to spread among BHK-21 cells. In addition, a gain of function-revertant virus was recovered with the Q2161A mutation after prolonged passage in cells.
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PMID:Amino acid substitutions in VP2 residues contacting sialic acid in low-neurovirulence BeAn virus dramatically reduce viral binding and spread of infection. 1255 11

We evaluated the role of gamma interferon (IFN-gamma) in protecting neurons from virus-induced injury following central nervous system infection. IFN-gamma(-/-) and IFN-gamma(+/+) mice of the resistant major histocompatibility complex (MHC) H-2(b) haplotype and intracerebrally infected with Theiler's murine encephalomyelitis virus (TMEV) cleared virus infection from anterior horn cell neurons. IFN-gamma(+/+) H-2(b) mice also cleared virus from the spinal cord white matter, whereas IFN-gamma(-/-) H-2(b) mice developed viral persistence in glial cells of the white matter and exhibited associated spinal cord demyelination. In contrast, infection of IFN-gamma(-/-) mice of the susceptible H-2(q) haplotype resulted in frequent deaths and severe neurologic deficits within 16 days of infection compared to the results obtained for controls. Morphologic analysis demonstrated severe injury to spinal cord neurons in IFN-gamma(-/-) H-2(q) mice during early infection. More virus RNA was detected in the brain and spinal cord of IFN-gamma(-/-) H-2(q) mice than in those of control mice at 14 and 21 days after TMEV infection. Virus antigen was localized predominantly to anterior horn cells in infected IFN-gamma(-/-) H-2(q) mice. IFN-gamma deletion did not affect the humoral response directed against the virus. However, the level of expression of CD4, CD8, class I MHC, or class II MHC in the central nervous system of IFN-gamma(-/-) H-2(q) mice was lower than those in IFN-gamma(+/+) H-2(q) mice. Finally, in vitro analysis of virus-induced death in NSC34 cells and spinal motor neurons showed that IFN-gamma exerted a neuroprotective effect in the absence of other aspects of the immune response. These data support the hypothesis that IFN-gamma plays a critical role in protecting spinal cord neurons from persistent infection and death.
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PMID:Gamma interferon is critical for neuronal viral clearance and protection in a susceptible mouse strain following early intracranial Theiler's murine encephalomyelitis virus infection. 1458 62

Nervous system infection with Borrelia burgdorferi frequently causes meningitis and rarely causes encephalomyelitis. Altered cognitive function also can occur in the absence of central nervous system infection. Recently developed serodiagnostic tools, such as the C6 assay, and appropriate use of Western blotting, promise to improve diagnostic accuracy. Treatment trials have demonstrated the efficacy of relatively brief courses of oral antimicrobial agents, even in peripheral nervous system infection and meningitis. Several well-performed studies have clearly shown that prolonged antimicrobial treatment of "post-Lyme disease" is ineffective. Diagnosis and treatment of Lyme disease continue to improve.
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PMID:Central Nervous System Lyme Disease. 1526 59

Nervous system infection with Borrelia burgdorferi frequently causes meningitis and rarely causes encephalomyelitis. Altered cognitive function also can occur in the absence of central nervous system infection. Recently developed serodiagnostic tools, such as the C6 assay, and appropriate use of Western blotting promise to improve diagnostic accuracy. Treatment trials have demonstrated the efficacy of relatively brief courses of oral antimicrobial agents, even in peripheral nervous system infection and meningitis. Several well-performed studies have clearly shown that prolonged antimicrobial treatment of "post-Lyme disease" is ineffective. Diagnosis and treatment of Lyme disease continue to improve.
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PMID:Central nervous system Lyme disease. 1626 55

Theiler's murine encephalomyelitis virus (TMEV), a member of the genus Cardiovirus, is an enteric pathogen of mice that causes acute encephalomyelitis followed by persistent central nervous system infection with chronic inflammation and demyelination after intracerebral inoculation. Although TMEV is a mouse pathogen, antibodies against TMEV strain GDVII have been detected in conventional rat colonies. Natural infection of rats by Cardiovirus has not yet been described. The purpose of this study was to demonstrate TMEV infection of rat colonies by using serologic assays, reverse transcription-polymerase chain reaction (RT-PCR) analysis, and clinical characterization. Indirect immunofluorescence assay of rat serum samples demonstrated antibodies against TMEV-GDVII in 86.3% of samples analyzed, and 77.2% of the antibody-positive samples had neutralizing antibodies. To determine whether rats can be infected experimentally with TMEV-GDVII, specific pathogen-free newborn mice and rats were inoculated intracerebrally with intestinal suspensions from seropositive rats. Both species showed the typical clinical signs of TMEV infection in mice, which is characterized by flaccid hindlimb paralysis and tremor. RT-PCR in brain tissue of experimentally infected animals detected RNA sequences corresponding to the 5' noncoding region of Cardiovirus known as the 'internal ribosome entry site.' These results suggest that rats can be naturally infected with TMEV and related Cardiovirus. Therefore, continued health monitoring for TMEV infection should be included in rat colonies mainly because these animals are used for various experimental purposes.
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PMID:Theiler's murine encephalomyelitis virus in nonbarrier rat colonies. 1627 Sep 3

Theiler's murine encephalomyelitis viruses (TMEV) are ubiquitous pathogens of mice, producing either rapidly fatal encephalitis (high-neurovirulence strains) or persistent central nervous system infection and inflammatory demyelination (low-neurovirulence strains). Although a protein entry receptor has not yet been identified, carbohydrate co-receptors that effect docking and concentration of the virus on the cell surface are known for both TMEV neurovirulence groups. Low-neurovirulence TMEV use alpha2,3-linked N-acetylneuramic acid (sialic acid) on an N-linked glycoprotein, whereas high-neurovirulence TMEV use the proteoglycan heparan sulfate (HS) as a co-receptor. While the binding of low-neurovirulence TMEV to sialic acid can be inhibited completely, only a third of the binding of high-neurovirulence TMEV to HS is inhibitable, suggesting that high-neurovirulence strains use another co-receptor or bind directly to the putative protein entry receptor. Four amino acids on the surface (VP2 puff B) of low-neurovirulence strains make contact with sialic acid through non-covalent hydrogen bonds. Since these virus residues are conserved in all TMEV strains, the capsid conformation of this region is probably responsible for sialic acid binding. A persistence determinant that maps within the virus coat using recombinant TMEV is also conformational in nature. Low-neurovirulence virus variants that do not bind to sialic acid fail to persist in the central nervous system of mice, indicating a role for sialic acid binding in TMEV persistence. Analysis of high-neurovirulence variants that do not bind HS demonstrates that HS co-receptor usage influences neuronal tropism in brain, whereas, the HS co-receptor use is not required for the infection of spinal cord anterior horn cells associated with poliomyelitis.
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PMID:Differential usage of carbohydrate co-receptors influences cellular tropism of Theiler's murine encephalomyelitis virus infection of the central nervous system. 1657 21


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