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

Theiler murine encephalomyelitis viruses (TMEVs) are picornaviruses that cause enteric and neurological disease in mice. The GDVII strain and other members of the GDVII subgroup are highly virulent and cause an acute, fatal polioencephalomyelitis following intracerebral inoculation, whereas the DA stain and other members of the TO subgroup cause a persistent, demyelinating infection. We previously produced a full-length, infectious DA cDNA clone. We now describe the generation of a full-length, infectious GDVII cDNA clone and the subsequent production of intratypic chimeric cDNAs and intratypic recombinant viruses. Inoculation of the recombinant viruses into mice demonstrated that a major determinant of TMEV neurovirulence is within the GDVII 1B (capsid protein VP2)-2C coding region, most likely in the GDVII 1B (VP2)-2A coding region. Genomic sequences 5' to this region of GDVII RNA also contribute to expression of the full neurovirulence phenotype. These data demonstrate the multigenic nature of TMEV neurovirulence, as has been reported for other viruses.
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PMID:Neurovirulence determinants of genetically engineered Theiler viruses. 216 33

An acute outbreak of encephalomyelitis in lions from a safari-park was investigated. Three moribund lions were euthanatized and a post mortem examination was performed. A disseminated non-suppurative polioencephalomyelitis with demyelination in the spinal cord was the only pathological finding. From tonsil material of one lion feline herpesvirus type 1 was isolated. Canine distemper virus, pseudorabies virus, feline infectious peritonitis virus and rabies were excluded as cause of the disease. The possible role of FHV-1 in etiology of the disease is discussed.
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PMID:A case report: encephalitis in lions. Pathological and virological findings. 231 36

The DA strain and other members of the TO subgroup of Theiler's murine encephalomyelitis viruses cause a persistent demyelinating infection, whereas the GDVII strain and other GDVII subgroup strains cause an acute lethal polioencephalomyelitis. We generated an infectious DA cDNA clone inserted into a transcription vector. Virus derived from transfection of transcripts produced a demyelinating disease indistinguishable from that of wild-type virus. The infectious clone provides a critical reagent for the production of interstrain recombinant viruses to help identify genetic loci responsible for the biological activities of the strains.
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PMID:Infectious cDNA clones of the DA strain of Theiler's murine encephalomyelitis virus. 255 69

Theiler's murine encephalomyelitis viruses (TMEV) belong to the Picornaviridae, and are divided into two subgroups. TO subgroup strains produce a persistent demyelinating central nervous system infection in mice, while GDVII subgroup strains cause acute polioencephalomyelitis. We generated three overlapping clones of the genome of DA strain, a member of TO subgroup. Sequence analysis revealed that the genome is 8093 nucleotides long with a poly(A) tail. The 5' noncoding region stretches from nucleotides 1 to 1065 and lacks a poly(C) tract. The open reading frame stretches from 1066 to 7968 and encodes 2301 amino acids. DA strain sequence is more closely related to members of the Cardiovirus genus than to members of other Picornavirus genera. Comparison with sequence of BeAn strain, another TO subgroup strain, showed that the P1 area has the greatest number of differences, while the noncoding regions are more well-conserved. The three overlapping clones will be important in recombinant infectious cDNA studies between strains of both subgroups.
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PMID:Molecular cloning and sequence determination of DA strain of Theiler's murine encephalomyelitis viruses. 283 72

Disease induced by 3 virulent strains of Canine Distemper Virus (CDV) was compared in specific pathogen-free Beagle dogs. All strains produced an encephalomyelitis but variation was observed in the severity, clinical course and resulting neuropathology. Infection with Snyder Hill strain of CDV was consistently acute; dogs either succumbed 14 to 19 days post-inoculation (PI) or recovered. Lesions in the neuraxis were those of a polioencephalomyelitis. In contrast, CDV strain A75-17 produced subacute to chronic disease in which demyelination was the predominant finding. Some dogs succumbed, generally around 28 to 42 days PI. Total recovery was again recorded for some members of the group. Others developed persistent central nervous system (CNS) infection but remained clinically stable until electively killed with barbiturate, up to 62 days PI. CDV strain R252 also induced delayed, predominantly white matter disease with a mixed pattern of mortalities, persistent infections and recoveries, similar to A75-17. Neutralizing antibody responses correlated with the disease course. Dogs which died had low serum titres or lacked serum antibody. Recovering dogs had the earliest and highest titres. A few dogs with persistent CNS infection had antibody in the cerebrospinal fluid also. Current concepts of the pathogenesis of canine distemper encephalomyelitis (CDE) are discussed and a basis for the strain-dependent clinical and pathological expression of CDE is proposed. Viral strain appears to be an important factor in this common disease of the canine CNS.
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PMID:Canine distemper encephalomyelitis: variation with virus strain. 669 31

The location and distribution of viral RNA were examined in the central nervous system tissues of weanling mice acutely infected with the GDVII strain of Theiler's murine encephalomyelitis virus. Viral RNA was detected by autoradiography following in situ hybridization of a 3H-labeled DNA synthesized in vitro complementary to purified viral RNA. Viral RNA was detected in pyramidal neurons of the hippocampus, cerebral cortex, brainstem nuclei, thalamus, basal ganglia, and spinal cord. Autoradiographic grains could be detected in the axonal and dendritic processes of many infected neurons. No viral RNA was detected in any cell of the cerebellum or white matter. In addition to demonstrating the location of viral RNA in infected central nervous system tissues, and hence the sites of viral replication during this acute polioencephalomyelitis, they indicate that necrosis of hippocampal neurons is due to lytic infection, rather than to hypoxia.
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PMID:Detection of Theiler's virus RNA in mouse central nervous system by in situ hybridization. 732 23

In 10 of 16 domestic cats with spontaneous non-suppurative encephalomyelitis, lesions were multifocal but relatively few and were considered nonspecific as to cause, although viral agents could not be excluded. Six cats had polioencephalomyelitis or polioencephalitis suggestive of viral infection. The clinical and morphological features are compared with those of previous reports of feline encephalitis possibly of viral origin. Some previously reported epidemiological and serological surveys suggest a possible role for arboviruses.
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PMID:Non-suppurative encephalomyelitis in cats suggestive of a viral origin. 746 77

Theiler's murine encephalomyelitis viruses (TMEV) are divided into two subgroups on the basis of their different biological activities. The GDVII strain produces acute polioencephalomyelitis in mice, whereas the DA strain produced demyelination with virus persistence in the spinal cord. A comparative study of GDVII and DA strains suggested that low host immune responses are responsible for the development of acute GDVII infection and that the persistence of infected macrophages plays a crucial role in the development of chronic white matter lesions in DA infection. All 78 mice infected with GDVII died or became moribund by day 13, while none of 54 mice infected with DA died. In the acute stage, the distribution of viral antigens in the central nervous system (CNS) tissue was similar in both GDVII and DA infections, although the virus titer was higher in GDVII infection. In DA infection, a substantial number of T cells were recruited to the CNS on day 6 when they were virtually absent in GDVII infection. The titer of neutralizing antibody was already high on day 6 in DA infection but was negligible in GDVII infection. Development of chronic paralytic disease from day 35 of the DA infection was accompanied by focal accumulation of viral antigen-positive macrophages in the spinal white matter. In addition, whiter matter lesions comparable to those in chronic DA infection were induced in the spinal cord within 7 days after intracerebral injection of DA-infected murine macrophages.
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PMID:A comparative study of acute and chronic diseases induced by two subgroups of Theiler's murine encephalomyelitis virus. 878 58

Theiler's murine encephalomyelitis virus (TMEV) strains are divided into two subgroups on the basis of their differing disease phenotypes. Members of the GDVII subgroup, such as GDVII strain, produce an acute lethal polioencephalomyelitis. In contrast, members of the TO subgroup, such as DA strain, induce a persistent infection with chronic demyelination; this white matter disease serves as an experimental model of multiple sclerosis (MS) due to their similar pathology and because the immune system in both diseases appears to contribute to the demyelination. The availability of full-length infectious TMEV clones, the relative simplicity of the TMEV genome, and the availability of the mouse as a host provide the opportunity to identify molecular determinants and disease mechanisms that are responsible for neurovirulence, demyelination and virus persistence, and makes this a valuable system for pathogenesis studies.
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PMID:Molecular determinants of Theiler's murine encephalomyelitis-induced disease. 879 98

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


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