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)

Infection with the Daniel strain of Theiler's murine encephalomyelitis (TMEV-DA) virus induces persistent demyelinating lesions in mice and serves as a model for multiple sclerosis. During the acute phase of the disease, however, viral infection leads to cell death in vivo. Viral-induced death may result directly from viral infection of neural cells, or indirectly, by activation of the immune system. To examine the direct effects of TMEV infection on neural cells, myelinated explant cultures of the murine cerebellum were infected with 10(5) pfu of TMEV-DA for periods ranging from 1 to 72 h. Our results indicate that TMEV-DA replicates in cultured neural tissue. Initially, viral antigen is localized to a few isolated neural cells. However, within 72 h antigen was observed in multiple foci that included damaged cells and extracellular debris. Viral infection led to a rapid and cyclical induction of necrosis with a time period that was consistent with the lytic phase of the viral life-cycle. Simultaneously, we observed an increase in apoptosis 48 h post-infection. Electron micrographic analysis indicated that viral-infected cultures contained cells with fragmented nuclei and condensed cytoplasm, characteristic of apoptosis. The localization of apoptosis to the cerebellar granule cell layer, identified these cells as presumptive granule neurons. Viral infection, however, did not lead to myelin damage, though damaged axons were visible in TMEV-infected cultures. These results suggest that during the acute phase of infection, TMEV targets neural cells for apoptosis without directly disrupting myelin. Myelin damage may therefore result from the activation of the immune system.
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PMID:Theiler's murine encephalomyelitis virus induces rapid necrosis and delayed apoptosis in myelinated mouse cerebellar explant cultures. 1085 78

The effect of eastern equine encephalomyelitis (EEE) virus on the survivorship of Aedes albopictus (Skuse), Anopheles quadrimaculatus Say, and Coquillettidia perturbans (Walker) was determined experimentally. Female mosquitoes were allowed to feed on EEE viremic chicks, and survival rates were compared for infected and uninfected mosquitoes. Additionally, the survival of female Cq. perturbans and An. quadrimaculatus intrathoracically (i.t.) inoculated with EEE was compared with controls receiving diluent inoculations. Infection with EEE significantly reduced survival in Cq. perturbans compared with uninfected individuals in per os infection experiments. I.t. infections of Cq. perturbans did not reduce survival when compared with diluent inoculated groups. In contrast, infection with EEE did not affect the survival of Ae. albopictus after per os infection or An. quadrimaculatus after either i.t. or per os infections.
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PMID:Effect of eastern equine encephalomyelitis virus on the survival of Aedes albopictus, Anopheles quadrimaculatus, and Coquillettidia perturbans (Diptera: Culicidae). 1100 81

Infection of susceptible mice with Theiler's murine encephalomyelitis virus results in neurological dysfunction from progressive central nervous system demyelination that is pathologically similar to the human disease, multiple sclerosis. We hypothesized that the development of neuropathology proceeds down a final common pathway that can be accurately quantified within a single spinal cord lesion. To test this hypothesis, we conducted quantitative ultrastructural analyses of individual demyelinated spinal cord lesions from chronically infected mice to determine whether pathological variables assessed within a single lesion accurately predicted global assessments of morphological and functional disease course. Within lesions we assessed by electron microscopy the frequencies of normally myelinated, remyelinated, and demyelinated axons, as well as degenerating axons and intra-axonal mitochondria. The frequency of medium and large remyelinated fibers within a single lesion served as a powerful indicator of axonal preservation and correlated with preserved neurological function. The number of degenerating axons and increased intra-axonal mitochondria also correlated strongly with global measures of disease course, such as total lesion load, spinal cord atrophy, and neurological function. This is the first study to demonstrate that functional severity of disease course is evident within a single demyelinated lesion analyzed morphometrically at the ultrastructural level.
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PMID:Quantitative ultrastructural analysis of a single spinal cord demyelinated lesion predicts total lesion load, axonal loss, and neurological dysfunction in a murine model of multiple sclerosis. 1102 39

To evaluate whether maternal illness following picornavirus infection during pregnancy adversely affects placental and fetal health, mice were inoculated with the GDVII strain of Theiler's murine encephalomyelitis virus or control cell lysate during days 4-7 of gestation. Gross appearance, histopathology and viral culture, and in situ hybridization positivity of placentae and fetuses from ill GDVII-infected, healthy GDVII-infected and control mice were compared. Twenty of 34 (59 per cent) GDVII-infected dams became clinically ill. More placenta-fetus pairs from ill mice were grossly abnormal (68 per cent) than from well GDVII-infected (51 per cent;P< 0.01) or control mice (9 per cent;P< 0.001). Virus was detected by in situ hybridization in 73 per cent of placentae and 29 per cent of fetuses from sick GDVII-infected dams, and in 85 per cent of placentae and 19 per cent of fetuses from healthy GDVII-infected mice (differences not significant). Histological abnormalities consisting of necrosis or an increase in hyaline tissue in the vascular labyrinth layer were similarly frequent in placentae from ill and well GDVII-infected mice (58 per cent versus 67 per cent, P=0.5). Viral RNA, inflammation and necrosis were evident in the heart, great vessels, brain and spinal cord of GDVII-infected fetuses. Infection with GDVII in early pregnancy produces a high rate of gross placental and fetal abnormalities. The rate of gross abnormalities exceeds the incidence of fetal infection and more closely parallels the rates of infection and histopathology in the placenta, suggesting that much of the damage to placenta-fetus pairs is a consequence of placental infection. In addition, the occurrence of viral-induced maternal illness is associated with additive risk to placental and fetal health not explained by an increased rate of placental or fetal infection.
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PMID:Picornavirus infection in early murine gestation: significance of maternal illness. 1109 34

Forty-eight children with disseminated demyelination of the CNS, 28 with acute disseminated encephalomyelitis (ADEM), seven with multiphasic disseminated encephalomyelitis (MDEM) and 13 with multiple sclerosis were studied for a mean follow-up period of 5.64 years. The presentation findings of the ADEM/MDEM group were compared with those of the multiple sclerosis group. The following findings were more commonly seen in ADEM/MDEM presentation compared with the multiple sclerosis presentations: predemyelinating infectious disease (74 versus 38%, P: < 0.05); polysymptomatic presentation (91 versus 38%, P: < 0.002); pyramidal signs (71 versus 23%, P: < 0.01); encephalopathy (69 versus 15%, P: < 0.002); and bilateral optic neuritis (23 versus 8%, not significant). Seizures occurred only in the ADEM/MDEM group (17 versus 0%, not significant). Unilateral optic neuritis occurred only in the multiple sclerosis patients (23 versus 0%, P: < 0.01). There were no differences in the frequencies of transverse myelitis, brainstem involvement, cerebellar signs and sensory disturbance between the two groups. ADEM/MDEM patients were more likely to have blood leucocytosis (64 versus 22%, P: < 0.05), CSF lymphocytosis (64 versus 42%, not significant) and CSF protein elevation (60 versus 33%, not significant). Patients presenting with multiple sclerosis were more likely to have intrathecal synthesis of oligoclonal bands on presentation (64 versus 29%, not significant). MRI showed that subcortical white matter lesions were almost universal in both groups, though periventricular lesions were more common in multiple sclerosis (92 versus 44%, P: < 0.01). By contrast, in ADEM/MDEM there was absolute and relative periventricular sparing in 56 and 78% of patients, respectively. Follow-up MRI revealed complete or partial lesion resolution in 90% and no new lesions in the ADEM/MDEM group. All of the multiple sclerosis patients had new lesions on repeat MRI (five during relapse and six during asymptomatic convalescent phases). The outcome in the ADEM patients was mixed; 57% of patients made a complete recovery. The mean follow-up for the 35 ADEM/MDEM patients was 5.78 years (range 1.0-15.4 years). Eight of the 13 multiple sclerosis patients relapsed within the first year; 11 had a relapsing-remitting course, one a primary progressive course and one a secondary progressive course. These differences in the presentation of ADEM/MDEM compared with multiple sclerosis may help in the prognosis given to families regarding the possibility of later development of multiple sclerosis.
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PMID:Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children. 1109 44

Rabies is a communicable disease that is almost always fatal. In its classic form, rabies is well recognized, but cases presenting with a paralytic illness mimic Landre's Guillain-Barre syndrome and in such cases the diagnosis remains in doubt. This problem is further compounded when the history of dogbite is not forthcoming. At autopsy rabies can be diagnosed by subjecting fresh tissue to virologic investigations or examining formalin-fixed paraffin-embedded tissue sections for the presence of characteristic inclusions; that is, the Negri bodies. However, these inclusions are not present in all cases. Hence, the need arises for a better method for diagnosis. The present study utilized immunohistochemistry as a diagnostic tool using both monoclonal and polyclonal antirabies antibodies in 20 cases of rabies encephalomyelitis. The diagnosis of rabies could be confirmed in 17 cases (85%) based on neuropathologic findings alone. In contrast, immunohistochemistry yielded positive results in all cases. Moreover, the amount of rabies viral antigen was much more abundant than could be expected from the histopathologic findings. Thus immunohistochemistry is a rapid, safe, sensitive and specific technique for the diagnosis of rabies.
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PMID:Immunohistochemical study of human rabies. 1113 35

Enterovirus (EV) can cause varied clinical manifestations. Involvement of the central nervous system (CNS) with the nonpolio EVs are common and important causes of morbidity in children. To investigate the manifestations of nonpolio enteroviral infections with CNS involvement during the EV outbreak, from February 1998 to January 1999, we collected 153 hospitalized patients in our pediatric ward caused by nonpolio EV infections which were diagnosed by history, clinical features, or detected from viral cultures. Fourteen patients (9.2%) had CNS presentations, 13 males and one female. The ages ranged from one month to 10.3 years. The spectrum of CNS presentations included aseptic meningitis (4 cases, 28.6%), encephalitis (5 case, 35.7%), encephalomyelitis (3 cases, 21.4%), and poliomyelitis-like syndrome (2 cases, 14.3%). Among these patients, 8 cases (57.1%) were isolated with EV71 from at least one site of rectal or throat swab sampling. Two fatal cases were presented as encephalitis and complicated with pulmonary edema. Generally, enteroviral infections are considered as a benign infectious disease in children. However, pediatricians should keep in mind that EV71 has caused several endemic outbreaks and continues to be an occasional cause of severe CNS disease. Early evaluation and appropriate treatment of CNS enteroviral infections may minimize the neurologic sequelae.
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PMID:Neurologic involvement in an outbreak of enterovirus 71 infection: a hospital-based study. 1127 Jan 82

Infection of SJL mice with wild-type BeAn strain of Theiler's murine encephalomyelitis virus (TMEV) leads to CD4(+)T cell-mediated CNS demyelination characterized by the development of anti-myelin epitope autoimmune responses via epitope spreading during the chronic stage of disease. To exmine the feasibility of virus-encoded mimic epitopes to initiate CNS autoimmunity, we recently developed a molecular mimicry model of virus-induced demyelinating disease wherein a non-pathogenic variant strain of TMEV was engineered to encode a 30-mer peptide encompassing the immunodominant myelin proteolipid protein, PLP139-151, epitope. SJL mice infected intracerebrally with TMEV encoding either the native PLP139-151 determinant or various peptide mimics of the epitope develop an early onset demyelinating disease mediated by activated PLP139-151-specific Th1 cells. The autoimmune nature of this early-onset demyelinating disease is shown by the fact that induction of tolerance to the PLP139-151 peptide prevents clinical disease and associated PLP139-151-specific T cell responses without affecting T cell reactivity to virus epitopes. Most significantly, TMEV encoding a molecular mimic peptide derived from the Haemophilus influenzae bacteria, homologous at only six out of thirteen of the core amino acids, led to CNS disease. These studies provide conclusive evidence that virus-induced myelin-specific autoreactive T cells can be induced by molecular mimicry and provide a useful model to study the disease inducing ability of viruses encoding human-disease-related mimicry peptides.
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PMID:Multiple pathways to induction of virus-induced autoimmune demyelination: lessons from Theiler's virus infection. 1133 86

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

Infection of susceptible mice with the low-neurovirulence Theiler's murine encephalomyelitis virus strain BeAn results in an inflammatory demyelinating disease similar to multiple sclerosis. While the majority of virus antigen is detected in central nervous system macrophages (Mphis), few infiltrating Mphis are infected. We used the myelomonocytic precursor M1 cell line to study BeAn virus-Mphi interactions in vitro to elucidate mechanisms for restricted virus expression. We have shown that restricted BeAn infection of M1 cells differentiated in vitro (M1-D) results in apoptosis. In this study, BeAn infection of gamma interferon (IFN-gamma)-activated M1-D cells also resulted in apoptosis but with no evidence of virus replication or protein expression. RNase protection assays of M1-D cellular RNA revealed up-regulation of Fas and the p55 chain of the tumor necrosis factor alpha (TNF-alpha) receptor transcripts with IFN-gamma activation. BeAn infection of activated cells resulted in increased caspase 8 mRNA transcripts and the appearance of TNF-alpha-related apoptosis-inducing ligand (TRAIL) 4 h postinfection. Both unactivated and activated M1-D cells expressed TRAIL receptors (R1 and R2), but only activated cells were killed by soluble TRAIL. Activated cells were also susceptible to soluble FasL- and TNF-alpha-induced apoptosis. The data suggest that IFN-gamma-activated M1-D cell death receptors become susceptible to their ligands and that the cells respond to BeAn virus infection by producing the ligands TNF-alpha and TRAIL to kill the susceptible cells. Unactivated cells are not susceptible to FasL or TRAIL and require virus replication to initiate apoptosis. Therefore, two mechanisms of apoptosis induction can be triggered by BeAn infection: an intrinsic pathway requiring virus replication and an extrinsic pathway signaling through the death receptors.
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PMID:Theiler's murine encephalomyelitis virus induces apoptosis in gamma interferon-activated M1 differentiated myelomonocytic cells through a mechanism involving tumor necrosis factor alpha (TNF-alpha) and TNF-alpha-related apoptosis-inducing ligand. 1139 May 94


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