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

The authors present the results of studying encephalomyelitis caused by the neurotropic (IHM) strain of the murine hepatitis virus in 60 mice of the C3H line infected intracerebrally at the age of 4 weeks. Morphological examinations of the brain carried out on the 5th-13th day (the acute period) and the 14th-30th day (the subacute stage) have shown that it is myelin-producing cells that are affected first in this form of encephalomyelitis, while the periaxonal process observed is a consequence of this affection. Proofs of this conclusion are presented. It is shown that in subacute encephalomyelitis, similar processes develop. Degeneration and infection of oligodendrocytes are not so pronounced in that case, as in the acute disease. However, destruction of even individual oligodendrocytes may lead (due to the peculiarities of their structure and function) to an avalanche-like process of demyelinization. It is supposed that the vesicular degeneration of myelin may arise in the sites of close contact between the myelin membranes and the cells of inflammation infiltrates (release of lysosomal enzymes and toxic products formed in edema). In the latter case the viruses serve as an antigen depot that causes and maintains the inflammatory process.
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PMID:[Demyelinization process in acute and subacute experimental encephalomyelitis]. 629 31

Visceral larva migrans was produced in 16 cynomolgus macaques (Macaca fascicularis) experimentally inoculated with 45,000 embryonated eggs of Toxocara canis as a single bolus or in 3 divided doses. The hematologic and serologic changes were similar to those observed in children with visceral Toxocara infection. Neurologic signs developed in 3 animals and were characterized by ataxia and nystagmus. Growth rates were diminished in inoculated animals when compared with the rates in noninoculated controls. Diagnostic antibody titers as measured by enzyme-linked immunosorbent assay were noted in all inoculated macaques by the 4th week, and these titers persisted during the 7-month period of observation. Antibody to Toxocara was not detected in the aqueous or vitreous humors. Lesions comprised severe granulomatous hepatitis and encephalomyelitis. Intraocular lesions associated with larval migration were not observed.
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PMID:Experimental Toxocara canis infection in cynomolgus macaques (Macaca fascicularis). 666 Jun 26

Clinical sarcocystosis was studied in 37 goats after inoculation with graded doses of sporocysts of Sarcocystis capracanis. Eight uninoculated goats served as controls. Clinical response varied with the dose. Goats inoculated with 10-40 million sporocysts died between 11 and 13 days after inoculation (DAI), from interstitial pneumonia, vasculitis, and necrosis of mesenteric lymph nodes. All goats inoculated with 100,000 or 1 million sporocysts died between 19 and 23 DAI; clinical signs were anorexia, fever (40-41 C), anemia, and weight loss. Four of 4 goats inoculated with 50,000 sporocysts and 1 of 4 inoculated with 10,000 sporocysts died 24, 28, 39, 68, and 61 DAI, respectively. Goats inoculated with 1,000 sporocysts and uninoculated goats remained clinically normal. After day 18 and before day 68, packed cell volume and hemoglobin content decreased to as low as 11% and 3.6 g/dl, respectively. Alanine aminotransferase and lactic dehydrogenase activities were inconsistently increased. Blood urea nitrogen and bilirubin values were increased, reaching as high as 63 mg/dl and 10 mg/dl, respectively. Histologically, thymic atrophy, vasculitis, hepatitis, cholangitis, myocarditis, generalized myositis, and encephalomyelitis were the main microscopic findings. The cause of the anemia in goats that died after day 19 was not determined.
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PMID:Sarcocystosis in goats: clinical signs and pathologic and hematologic findings. 678 65

Demyelination processes due to viral infections (encephalomyelitis induced by mouse hepatitis virus, Theiler's encephalomyelitis, canine distemper, and marek's disease) were simulated in laboratory animals to study the corresponding human diseases (multiple sclerosis, multifocal leucoencephalopathy, Guillain-Barre's syndrome). The following mechanisms of tissue injury are discussed: (1) viral damage of myelin-supporting cells, (2) demyelination occurring as a side effect of specific and non-specific inflammatory reactions to the viruses persisting in the nervous system, (3) autoimmune reaction triggered by virus infection. Special attention is paid to the role of virus agents in the development of these processes.
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PMID:[Demyelinating processes of a viral nature]. 703 82

Ten inbred strains of mice were tested for their susceptibility to experimental allergic encephalomyelitis (EAE) after sensitization with mouse spinal cord in complete Freund's adjuvant followed by booster injections of Bordetella pertussis. The results extended previous findings in that not all susceptible mice possessed the H-2s haplotype, but mice with an H-2q background (DBA1/J strain) were also susceptible. Neuropathologic examination of experimental allergic encephalomyelitis in the mouse showed that from strain to strain, the condition was similar. The over-all pathologic picture was somewhat midway between that seen in other species sensitized with whole nervous tissue in complex Freund's adjuvant and hyperacute experimental allergic encephalomyelitis in rats similarly sensitized but with the addition of B. pertussis. Perivascular cuffing, though present, was less pronounced than in other species. There was a prominent polymorphonuclear response, and extravasation of fibrin and red cells occurred. Primary demyelination was a transient, early feature of the disease process in mice, but nerve fiber depletion and gliosis occurred as the disease progressed. The observed myelin degradation most commonly involved the ingestion by macrophages of small fragments of dissociated myelin via crypts or infoldings of the cell surface, at the bases of which were pinocytic, coated vesicles. A similar pattern of myelin breakdown has been described in mouse hepatitis virus encephalomyelitis and multiple sclerosis.
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PMID:Neuropathology of experimental allergic encephalomyelitis in inbred strains of mice. 740 30

Materials of autopsies of 52 children suffering from severe herpetic infection, intrauterine as a rule, were analysed. The etiology of the process was proved by immunofluorescent and serological examinations. The disease was markedly generalized, however, with predominant involvement of the liver, lungs, and central nervous system of the type of pneumonia, hepatitis and encephalomyelitis. Early in the disease, changes of alveolocytes, hepatocytes, and other epitheliocytes were observed, consisting primarily in a peculiar alteration of their nuclei. Simultaneously, moderate signs of inflammation were observed, but in most severe cases it was alterative.
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PMID:[Pathological anatomy of a herpes infection caused by herpes simplex type 2 virus in infants]. 744 39

Mice infected with the neurotropic JHM strain of mouse hepatitis virus (MHV-JHM) develop a demyelinating encephalomyelitis several weeks after infection. Astrogliosis and infiltration of inflammatory cells are prominent findings in the brains and spinal cords of infected mice. In this report, astrocytes in infected spinal cords were analyzed for expression of three pleiotropic cytokines, TNF-alpha, IL-1 beta, and IL-6; Type 2 nitric oxide synthase (iNOS); and MHC class I and II antigen. The data show that all three cytokines and iNOS are expressed by astrocytes in chronically infected spinal cords. These activated astrocytes are localized to areas of virus infection and demyelination, although most of the astrocytes expressing these proteins are not MHV-infected. MHC class I and II antigen can be detected in these spinal cords as well, but not in cells with the typical morphology of astrocytes. TNF-alpha, IL-6, and iNOS are also evident in the brains of mice with MHV-induced acute encephalitis, but in marked contrast to the results obtained with the chronically infected mice, most of the cells expressing these cytokines or iNOS had the morphology of macrophages or other mononuclear cells and very few appeared to be astrocytes. Additionally, astrocytes and, most likely, oligodendrocytes are infected in the spinal cords of mice with chronic demyelination. These results are consistent with a role for both viral infection of glial cells and high localized levels of proinflammatory cytokines and nitric oxide in the demyelinating process in mice infected with MHV-JHM. They also show that analogously to the human demyelinating disease, multiple sclerosis, astrocytes are a major cellular source for these cytokines in mice with chronic, but not acute disease.
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PMID:Activation of astrocytes in the spinal cord of mice chronically infected with a neurotropic coronavirus. 749 73

Molecular mimicry has been characterized as the presence of common epitopes, either linear or conformational, shared by host and microbial determinants. Such cross-reactivity may lead to an autoimmune disease. On the other hand molecular mimicry between certain viral proteins and host determinant may protect invading virus to be eliminated by immune system and may promote persistence. In this mini-review I discuss the molecular mimicry of S peplomer protein of mouse hepatitis virus, strain JHM (MHV-JHM) to the host Fc gamma receptor (Fc gamma R). MHV-JHM induces in rodents acute encephalomyelitis and surviving animals develop demyelinating disease with concomitant persistent infection. We have demonstrated that rabbit IgG, but not is F(ab')2 fragments, monoclonal rat and mouse IgG and the rat 2.4G2 anti-Fc gamma R mab immunoprecipitated natural and recombinant S peplomer protein of several strains of MHV. Furthermore, MHV-JHM infected cells formed rosettes with anti-sheep red blood cell (SRBC) - antibody coated SRBC. The 2.4G2 anti-Fc gamma R mab are able to neutralize several strains of MHV, presumably by binding to S peplomer protein. Therefore, the Fc binding site of S is present on the surface of MHV-infected cells. This molecular mimicry between S peplomer protein of MHV-JHM and Fc gamma R has been extended to other members of Coronaviridae, namely bovine coronavirus and transmissible gastroenteritis virus but not to infectious bronchitis virus. The molecular mimicry of viral antigens to Fc receptors has been described also for members of Herpesviridae, namely Herpes simplex, cytomegalovirus and Varicella zoster.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular mimicry between Fc receptors and viral antigens. 750 51

Neutralizing anti-tumor necrosis factor alpha (TNF-alpha) antibody treatment of mice infected with the neurotropic JHMV strain of mouse hepatitis virus showed no reduction of either virus-induced encephalomyelitis or central nervous system demyelination. TNF-alpha-positive cells were present in the central nervous system during infection; however, TNF-alpha could not be colocalized with JHMV-infected cells. In vitro, TNF-alpha mRNA rapidly accumulated following JHMV infection; however, no TNF-alpha was secreted because of inhibition of translation. Both live and UV-inactivated virus inhibited TNF-alpha secretion induced by lipopolysaccharide. These data show that TNF-alpha is not secreted from infected cells and indicate that if contributes to either JHMV-induced acute encephalomyelitis nor primary demyelination.
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PMID:Tumor necrosis factor expression during mouse hepatitis virus-induced demyelinating encephalomyelitis. 763 37

The genomic relationship of porcine hemagglutinating encephalomyelitis virus (HEV) to bovine coronavirus (BCV) and human coronavirus (HCV) strain OC43 was examined by dot blot hybridization assays. Two BCV S gene-specific probes were generated by polymerase chain reaction from the avirulent L9-strain of BCV. Probes were located in the S1 and the S2 region of the peplomeric (S) glycoprotein gene. The S1 probe (726 bp) hybridized with BCV and HCV-OC43, but not with HEV under moderate stringency hybridization conditions (50 degrees C). Only slight signals were present with mouse hepatitis virus (MHV) and no signals were observed with feline infectious peritonitis virus (FIPV) or canine coronavirus (CCV). At high stringency conditions (60 degrees C) the S1 probe hybridized with BCV only. Using the S2 probe (680 bp) under moderate stringency conditions, hybridization signals were obtained with BCV, HCV-OC43 and HEV (strains 67N, NT9, VW572). The signals obtained by the three HEV strains were altogether weaker than with BCV and HCV-OC43. The S2 probe did not react with MHV, FIPV and CCV. At high stringency the S2-specific probe hybridized with BCV and HCV-OC43 but did not hybridize with HEV. Nucleotide sequence analysis of the region covering the S2 probe in HEV revealed 92.6% nucleotide sequence homology to BCV and 91.9% to HCV-OC43. In contrast, the region covering the S1 probe in HEV could not be amplified using the BCV S1-specific primers. The hybridization and sequencing results thus indicate a closer genomic relationship between BCV and HCV-OC43 than there is between HEV and BCV or HCV-OC43 respectively.
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PMID:Genomic relationship of porcine hemagglutinating encephalomyelitis virus to bovine coronavirus and human coronavirus OC43 as studied by the use of bovine coronavirus S gene-specific probes. 764 53


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