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

Theiler's murine encephalomyelitis viruses (TMEV) are serologically related picornaviruses which cause both enteric and neurological disease in mice. The biological activities of TMEV vary between the two different TMEV subgroups (TO and GDVII) and with different passage histories of the same TMEV strain (e.g., mouse brain-passed versus tissue culture-passed DA strain of the TO subgroup). We raised neutralizing monoclonal antibodies (mAbs) against tissue culture-passed DA and GDVII strains of TMEV. We produced two mAbs against the DA strain which neutralized all members of the TO subgroup, but not the GDVII subgroup strains (GDVII and FA); these two DA mAbs reacted similarly with both mouse brain-passed DA and tissue culture-passed DA. Of six neutralizing GDVII mAbs, four reacted only to GDVII and FA, whereas two neutralized TO strains as well. These mAbs demonstrate the presence of TMEV group-specific as well as subgroup-specific neutralization and substantiate the division of TMEV into two distinct subgroups. On Western immunoblots one of the two DA mAbs reacted against isolated DA VP1, two GDVII mAbs (which were TMEV group specific) reacted against isolated GDVII VP1 and DA VP1, and the other DA mAb and four other GDVII mAbs required an intact virion conformation for reactivity. An analysis of the epitopes recognized by these mAbs may elucidate sites important in TMEV biological activities.
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PMID:Neutralizing monoclonal antibodies to Theiler's murine encephalomyelitis viruses. 257 78

Canine distemper encephalomyelitis is an important neurological disease of the dog and is also of comparative medical interest. With some viral strains, demyelinating encephalomyelitis is seen; whether or not oligodendrocyte infection occurs has remained controversial. By examining very early white matter lesions unequivocal oligodendrocyte infection has been identified. Accordingly the direct effect of virus on oligodendrocyte viability must be weighed in considering the pathogenesis of this canine CNS infection.
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PMID:Evidence of oligodendrocyte infection and degeneration in canine distemper encephalomyelitis. 271 48

1. Maternal antibody protected C57BL/6 and BALB/c suckling mice from the acute, fatal encephalomyelitis caused by MHV-JHM. 2. 40% of the C57BL/6 mice and 25% of the BALB/c mice which were protected by maternal antibody developed neurological disease days to weeks later. Although the clinical syndromes developed by the two different strains were different, in both cases the mice developed a demyelinating encephalomyelitis with fewer inflammatory changes present in the grey matter. 3. Presence or absence of neutralizing antibody in the sera of maternal antibody-protected C57BL/6 mice did not correlate with the development of clinically evident neurological disease. 4. Infectious virus could only be isolated from C57BL/6 mice with neurological disease, although viral antigen could be detected in most mice whether symptomatic or not. 5. This model should be useful for the study of the viral and immune factors important in MHV-induced viral demyelination.
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PMID:Maternal antibody-modulated MHV-JHM infection in C57BL/6 and BALB/c mice. 282 43

A survey was conducted by testing 115 paired equine serum and cerebrospinal fluid samples by hemagglutination-inhibition for antibodies to Powassan and snowshoe hare viruses, and by virus neutralization for antibodies to equine herpesvirus type 1. Twenty-five samples were from horses with spontaneous neurological disease and the remainder from horses euthanized because of various nonneurological disorders. All sera and cerebrospinal fluids were negative for antibodies to Powassan virus. Fifty-one sera (44.3%) and 15 cerebrospinal fluids (13.0%) had antibodies to snowshoe hare virus. Ninety-eight sera (85.2%) and four cerebrospinal fluids (3.5%) were positive for antibodies to equine herpesvirus type 1. Powassan virus was inoculated intracerebrally into one, and intravenously into four ponies. Neurological signs associated with a nonsuppurative encephalomyelitis occurred in three ponies. Antibodies to Powassan virus were detected in sera of all animals but in cerebrospinal fluids of only two. Powassan virus was isolated from brain and spinal cord of only the intracerebrally inoculated animal.
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PMID:Agents of equine viral encephalomyelitis: correlation of serum and cerebrospinal fluid antibodies. 283 46

The presence of maternal antibodies protected suckling C57BL/6 mice from the clinical manifestations of the acute encephalomyelitis caused by mouse hepatitis virus, strain JHM (MHV-JHM), a coronavirus, even though histological evidence of encephalomyelitis was found at early times after inoculation. 100% of infected suckling mice developed a fatal disease in the absence of maternal antibody. By 14 days after inoculation, the brains of all antibody-protected mice examined were nearly normal on histological examination. At 3-8 weeks post-inoculation, approximately 40% of the antibody-protected mice developed a neurological disease characterized by hindlimb paralysis and wasting. Evidence of inflammation and demyelination was apparent in the spinal cord and brainstem. The mice that remained asymptomatic at this time showed few signs of inflammation and none developed clinical disease over the following 9 months. Viral antigen could be detected in most of the mice examined at all times after inoculation, whether symptomatic or not, and was particularly evident in the animals with hindlimb paralysis. MHV-JHM could be consistently cultured from the mice with hindlimb paralysis. These results show that maternal immune factors can completely protect susceptible mice from the acute, fatal, clinical encephalomyelitis caused by MHV-JHM, but cannot prevent the establishment of a latent state and subsequent development of virus-induced, clinically evident, demyelinating disease. This model will be useful for studying the virus and host factors important for the development of MHV-JHM latency and subsequent virus-induced demyelination.
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PMID:Late onset, symptomatic, demyelinating encephalomyelitis in mice infected with MHV-JHM in the presence of maternal antibody. 285 74

"Remote effects" of cancer on the nervous system (paraneoplastic syndromes) are disorders of the nervous system of unknown cause that occur almost exclusively, or with greatly increased frequency, in patients with identifiable or occult cancer. There are several hypotheses concerning the pathogenesis of these rare disorders. One hypothesis is that the underlying tumor and portions of the nervous system share antigens and that an autoimmune response generated against the tumor causes the nervous system disorder. Evidence supporting this hypothesis includes the ability to transmit the Lambert-Eaton Syndrome (a paraneoplastic syndrome involving the neuromuscular junction) to experimental animals by infusing IgG from patients with the disorder, the presence of autoantibodies against Purkinje cell neurons in some patients with paraneoplastic cerebellar degeneration, and the presence of autoantibodies against many neurons in patients with sensory neuronopathy and encephalomyelitis. Other evidence supporting the hypothesis is presented in this review.
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PMID:Autoimmune pathogenesis of paraneoplastic neurological syndromes. 331 39

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

Two children are described with postnatally acquired acute rubella which induced neurological disease. The first patient with restricted transverse myelitis (Th 11-12) was remarkable for the positive result obtained by the magnetic response (MR) technique of the spinal cord. In the second patient the clinical examination demonstrated a circumscribed, however severe, lasting defect in the extrapyramidal motor system with facial muscle dystonia and complete anarthria; in the latter case the CSF contained rubella specific IgM five days after the onset of exanthema. No abnormalities were noticed by MR five weeks after the clinical onset. The possible significance of MR imaging in virus-induced encephalomyelitis is discussed.
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PMID:Rubella myelitis and encephalitis in childhood. A report of two cases with magnetic resonance imaging. 360 Oct 2

JHM virus, when inoculated into neonatal rats, can cause either a rapidly fatal acute encephalomyelitis or, after longer incubation periods, a paralytic disease. The cerebrospinal fluid (CSF) and serum anti-JHM virus IgG concentrations present in rats prior to onset of clinical symptoms or during the acute and paralytic phases of disease were compared. High CSF/serum ratios, indicative of local antibody production in the CNS, were noted only where disease was demonstrable suggesting that local antibody production accompanied the infection but did not prevent the neurological disease. Among animals in which neurologic symptoms had not become manifest, only those with elevated CSF/serum ratios were found to have histological CNS lesions. Immunofluorescent microscopy indicated that viral antigens were present in both glia and neurons. Antigen-positive cells were frequently present in histologically normal CNS tissue, while regions of necrosis were antigen negative. Testing for the presence of viral RNA with JHM cDNA probes revealed that the virus was rapidly disseminated throughout the CNS, presumably establishing centers of infection prior to the development of recognizable tissue damage. Viral RNA was also detected in the CNS following recovery from paralysis and as late as 5 months postinfection, where no disease occurred. These findings indicate that, although infection by JHM virus can spread rapidly throughout the CNS, formation of lesions during chronic disease is a slower process. The current data and previous observations suggest that JHM virus can remain in a latent state for periods of at least several months in rats without apparent neurologic disease despite the absence of any known provirus phase in the replicative strategy of coronaviruses.
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PMID:In vivo and in vitro models of demyelinating disease. IX. Progression of JHM virus infection in the central nervous system of the rat during overt and asymptomatic phases. 609 33

Theiler's murine encephalomyelitis virus (TMEV) is an enteric pathogen of mice which causes acute and chronic neurological disorders in the natural host. When brain-derived stocks of TMEV isolates are adapted to cell culture they predominantly form either large or small plaques. In this study the type of central nervous system (CNS) infection (acute versus chronic) and the associated disease occurring in mice inoculated intracerebrally with large and small plaque strains of TMEV was investigated. Large and small plaque strains of TMEV were found to vary in virulence, type of neurological disease produced and ability to establish persistent CNS infection in mice. Two large plaque strains, GDVII and FA viruses, were highly virulent, produced acute encephalitis, but were cleared from the nervous systems of surviving animals. Therefore, it appears that these large plaque variants do not cause persistent CNS infection in mice. In contrast, five small plaque strains, DA, WW, TO4, Yale and BeAn8386 viruses, were relatively avirulent, usually produced no illness during the first month after inoculation, but readily established persistent CNS infection in mice. Persistently infected mice later developed demyelinating disease. Having identified strains of TMEV that differ regarding their ability to persist, we now hope to be able to exploit this difference in elucidating the basic mechanism(s) of TMEV persistence.
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PMID:Persistent Theiler's murine encephalomyelitis virus infection in mice depends on plaque size. 624 40


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