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)

The effects of herpes simplex virus type 1 (HSV-1) infection on the course of experimental allergic encephalomyelitis (EAE) were studied in rats. Fifty percent of animals given two intracerebral injections of HSV-1, one before and one after induction of EAE, showed clinical and pathologic evidence of recently exacerbated EAE 16 days after the second HSV-1 injection. When HSV-1 injections were administered subcutaneously before and after induction of EAE, 45% of survivors showed pathologic changes of recent EAE. A single injection intracerebally or subcutaneously of HSV-1 given before the development of EAE did not change the clinical severity or time course of EAE. A single injection intracerebrally or subcutaneously of HSV-1 given after the development of EAE did not cause clinical recrudescence of the EAE. Pathologic but not clinical evidence of EAE recurrence was found in three of nine animals given one injection of HSV-1 intracerebrally before and one of control material intracerebrally after induction of EAE. Pathologic evidence of EAE recurrence was found in six of 14 rats given one injection of control material intracerebrally before and one of HSV-1 intracebrally after induction of EAE. Cell suspensions, free of HSV-1, given prior and subsequent to the development of EAE did not cause a change in the EAE severity or a recrudescence of the EAE.
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PMID:Herpes simplex infection and experimental allergic encephalomyelitis. An experimental model system for reactivation of EAE. 55 69

Herpes simplex virus was injected into the vitreous of suckling and adult rabbits. In the suckling rabbits the infection caused an arrested myelination of the strip. Further, the infected strips showed degenerative changes with splitting and distension of myelin sheaths which then disintegrated. Ultrastructurally, herpes simplex virus particles were found in both oligodendroglial cells and in astrocytes in the bundles. No increase in intraocular pressure was recorded during the inflammation. The infection spread along optic pathways to the opposite side. Inflammatory cells appeared at the surface and infiltrated the degenerating strip. Especially in the contralateral eye, an extensive inflammatory cell infiltration was seen among bundles of nerve fibres which showed partly well-preserved myelin and partly with signs of demyelination reminiscent of the picture of experimental allergic encephalomyelitis in the epiretinal strip.
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PMID:Arrest of myelination and demyelination in rabbit retina induced by herpes simplex virus infection. 68 60

T cell sensitization to two myelin components, myelin basic protein (MBP) and myelin proteolipid protein (PLP), may be important to the pathogenesis of multiple sclerosis (MS). Using the limiting dilution assay, we demonstrated that the blood of MS patients had an increased frequency of MBP-reactive T cells compared with normal subjects and patients with other neurological diseases (OND) and rheumatoid arthritis. There was no difference in T cell frequency to a synthetic peptide, PLP139-151, or Herpes simplex virus. Within cerebrospinal fluid (CSF), 37% of IL-2/IL-4-reactive T cell isolates from MS patients responded either to MBP or PLP139-151 while only 5% of similar isolates from OND patients responded to these myelin antigens. The mean relative frequency of MBP-reactive T cells within CSF from MS patients was significantly higher than that of OND patients (22 x 10(-5) cells versus 1 x 10(-5) cells) and was similar to that of MBP reactive T cells within the central nervous system of rats with experimental autoimmune encephalomyelitis. These results lend new support to the hypothesis that myelin-reactive T cells mediate disease in MS.
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PMID:Frequency of T cells specific for myelin basic protein and myelin proteolipid protein in blood and cerebrospinal fluid in multiple sclerosis. 137 22

Immunohistochemistry was used to study herpes simplex virus type 1-induced central nervous system demyelination in the trigeminal root entry zone of mice inoculated with herpes simplex virus type 1 by the corneal route. There was no change in peripheral nervous system myelin as shown by immunostaining for P0 glycoprotein. Double immunoperoxidase staining for herpes simplex virus type 1 antigens and glial fibrillary acidic protein showed that most of the infected cells were astrocytes. Glial fibrillary acidic protein immunostaining was completely lost in the inferior medial portion of the trigeminal root entry zone at 6 days after herpes simplex virus type 1 inoculation, a time when central nervous system myelin was preserved as indicated by immunostaining for myelin basic protein. The pattern of glial fibrillary acidic protein staining did not change and herpes simplex virus type 1 antigens were no longer detected after day 8. There was a progressive loss of myelin basic protein staining within the area unstained by glial fibrillary acidic protein antisera on days 8 to 14. This pattern of astrocyte loss before central nervous system demyelination is strikingly different from the reactive astrocytosis seen in other demyelinating lesions, such as acute experimental allergic encephalomyelitis, progressive multifocal leukoencephalopathy, or acute multiple sclerosis. Herpes simplex virus type 1 infection in mice provides an unusual model of acute central nervous system demyelination preceded by a loss of astrocytes.
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PMID:Early loss of astrocytes in herpes simplex virus-induced central nervous system demyelination. 204 45

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease which is associated with persistent virus infection of the central nervous system. To study the interaction between TMEV and host cells, we infected the G26-20 glioma cell line in vitro, and this resulted in a lytic infection in which most, but not all, cells were killed. Surviving cells divided and formed a viable monolayer in which a small proportion of cells displayed viral cytopathic effects. Levels of virus produced by these cultures over a 6 month period fluctuated between 6 and 8 log10 p.f.u./ml as measured by viral plaque assay. Similarly, the percentage of cells producing both viral antigen and viral RNA, as measured by a simultaneous immunoperoxidase/in situ hybridization technique, varied between 5 and 30%. Although persistently infected cultures were susceptible to challenge by both vesicular stomatitis virus and herpes simplex virus, they were resistant to infection by homologous viruses. Interferon activity was not identified. TMEV isolated from passage 12 produced smaller plaques than wild-type Daniels strain virus (wt-DAV) on L-2 cell monolayers. In contrast to demyelination induced in SJL/J mice after intracerebral inoculation with wt-DAV, mice infected with the small plaque variant virus failed to develop viral persistence or chronic demyelination. However, following immunosuppression by total body irradiation, SJL/J mice infected with the small plaque variant developed viral persistence but no demyelination. Characterization of the biochemical and molecular determinants of the variant will lead to a better understanding of determinants important in viral persistence.
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PMID:Persistent infection of a glioma cell line generates a Theiler's virus variant which fails to induce demyelinating disease in SJL/J mice. 221 94

The effect of cimetidine on survival was investigated in mice infected with herpes simplex virus type 2 (HSV-2), murine encephalomyelitis virus (GD-VII), and vesicular stomatitis virus (VSV). BALB/c mice, 5 weeks of age, were injected intraperitoneally (i.p.) with 5.5 x 10(5) plaque-forming units (PFU) of virus/0.5 ml, and cimetidine (1 mg/0.5 ml) was administered simultaneously. The survival rates of 80% and 85% in the cimetidine groups were significantly greater than the 10% and 23% for the control groups. The GD-VII- and VSV-infected control mice were dead at 3 days after virus inoculation. However, more cimetidine-treated mice survived than control mice. When anti-mouse T-cell serum or cyclosporine, which is a helper T-cell suppressor, was administered to BALB/c mice; the effect of cimetidine against the HSV-2 infection could be observed. When injected with anti-asialo GM1, BALB/c mice or beige mice with low natural killer (NK) cell activity were not affected by cimetidine. Lastly, cimetidine was shown to activate the cytotoxic action on NK cells. The above results indicate that the antiviral effects of cimetidine depend on NK cell activation.
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PMID:The effect of cimetidine on survival of mice infected with herpes simplex virus type 2, murine encephalomyelitis virus and vesicular stomatitis virus infections. 256 3

Four murine anti-idiotypic (a-Id) hybridoma antibodies were produced against immunoglobulins (Ig) present in the cerebrospinal fluid (CSF) obtained from an MS patient 2 mo after the onset of disease. The four a-Id antibodies were shown to delineate idiotopes present on three distinct Ig subpopulations designated ID-19, ID-40, and ID-97. All three Ig subpopulations were produced in part by intrathecally localized B cells, together making up approximately 5% of the total CSF-Ig 2 mo after the onset of disease. Longitudinal analysis of the concentration of these Ig subpopulations in CSF showed that two subpopulations, ID-40 and ID-97, exhibited a regular relation to the clinical course of the disease, i.e., were decreased (ID-40) or increased (ID-97) in the first CSF sample obtained after two consecutive exacerbations. Screening of sera from 52 optic neuritis patients and 51 heterologous MS patients revealed that one MS patient's serum contained an Ig subpopulation that was idiotypically cross-reactive with ID-97. So far, screening of these Ig subpopulations for reaction with several viruses (measles, parainfluenza type 1, influenza type A, cytomegalovirus, herpes simplex virus, rubella virus, poliovirus, murine encephalomyelitis viruses, and reovirus) and myelin basic protein has failed to reveal their antigen specificities.
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PMID:Longitudinal analysis of three intrathecally produced immunoglobulin subpopulations in an MS patient. 257 10

In the brains and spinal cords of 153 adult patients dying with acquired immunodeficiency syndrome (AIDS) at New York and Memorial Hospitals a subacute encephalitis with multinucleated cells was present in 28% of all patients. This encephalitis was characterized by multinucleated cells primarily located in the white matter and associated with myelin pallor and sparse infiltrates of rod cells, macrophages, gemistocytic astrocytes and lymphocytes. The incidence per 12 month period ranged from 0 to 43% and significantly increased between 1983-84 (14%) and 1984-85 (43%). Recent virologic and pathologic studies suggest that this encephalitis may be caused by direct LAV/HTLV-III infection of the central nervous system (CNS). Cytomegalovirus encephalomyelitis and toxoplasmosis were the most common opportunistic infections (26% and 10%, respectively). Progressive multifocal leukoencephalopathy, herpes simplex ventriculitis, varicella-zoster leukoencephalitis and fungal infections were infrequent (less than 3% each). A nonspecific encephalitis with microglial nodules and with mild white matter changes occurred in 17%, vacuolar myelopathy in 29% and CNS lymphoma in 6%. Less than 20% of patients had either normal brains or terminal metabolic encephalopathies. This survey shows that neuropathologic complications of AIDS are frequent. Infections are the most common complication and are caused by probable LAV/HTLV-III infection, or by opportunistic organisms.
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PMID:Neuropathology of acquired immunodeficiency syndrome (AIDS): an autopsy review. 302 14

Non-genital herpes simplex virus in immunocompetent hosts causes a variety of primary infections--gingivostomatitis, keratoconjunctivitis, herpetic whitlow, and encephalomyelitis. Recurrent infections with orolabialis are very common, but are usually mild and self-limiting. Cutaneous complications of herpes simplex virus infections include eczema herpeticum and erytherma multiforme. Systemic treatment with acyclovir is indicated in encephalomyelitis, progressive eczema herpeticum, and frequent severe erythema multiforme. Chronic, suppressive acyclovir treatment may be helpful in severe recurrent infections or those complicated by erythema multiforme/dissemination. Many primary and recurrent infections can be treated with simple topical therapy to control secondary infection. There is no evidence that systemic treatment affects viral latency or recurrent infections following discontinuation of treatment.
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PMID:Management of non-genital herpes simplex virus infections in immunocompetent patients. 304 90

In recent years, herpes simplex virus has been recognized as an important CNS pathogen in neonates and adults. The recent development of effective antiviral therapy has substantially reduced the excessive morbidity and mortality associated with these infections. For neonatal herpes simplex infections, the current drug of choice is vidarabine. The results of ongoing clinical trials comparing vidarabine with acyclovir in neonatal herpes may lead to a change in the recommended therapy. In the adult, the therapy of choice for herpes simplex encephalitis is acyclovir. Although effective, the present therapies for herpes simplex infections of the CNS leave much room for improvement. In addition to the development of more effective antiviral drugs and less invasive diagnostic techniques, prevention of these often devastating infections will be important in reducing morbidity and mortality. The CNS diseases associated with varicella and herpes zoster may have a different pathogenesis. The implication for therapy in these diseases favors nonspecific supportive therapy in the varicella-associated syndromes. The few anecdotal reports of the use of vidarabine and acyclovir in herpes zoster encephalitis and the histopathologic evidence suggesting viral invasion of the CNS in many cases of zoster-associated neurologic syndromes makes the use of specific antiviral therapy in zoster encephalomyelitis more rational. However, appropriate therapeutic recommendations will have to be based on controlled clinical trials that have not yet been performed.
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PMID:CNS diseases associated with varicella zoster virus and herpes simplex virus infection. Pathogenesis and current therapy. 352 4


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