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)

A prolongation in the lives of Swiss mice inoculated intracerebrally with lymphocytic choriomeningitis virus (LCM) was observed after treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). A variety of treatment schedules, including therapy once or twice daily up to 17 days and single treatments at various times after virus inoculation, were employed. Virus titers ranging to greater than 10(4) were detected in the blood and brains of surviving drug-treated animals. In three comparative studies in which different treatment schedules were used, BCNU was shown to exert a protective effect approximately equal to that of methotrexate in LCM virus-infected mice. Tests were also carried out to investigate the activity of BCNU in mice experimentally infected with eastern equine encephalomyelitis (EEE) virus, western equine encephalomyelitis virus, Semliki Forest (SF) virus, herpes simplex virus, influenza virus strain PR8, vaccinia virus strain WR, Rous sarcoma virus, Friend leukemia virus (FLV), and poliovirus. Slight increases in life span were observed in the treated EEE, SF, and influenza PR8 virus-infected animals. Significant reduction in splenomegaly in FLV-infected animals treated with BCNU was demonstrated. The possible mechanisms of LCM virus inhibition by BCNU, on the basis of these and other studies, were postulated to be either specific antiviral activity or inhibition of "lethal" immune response to the LCM virus. Each of these postulates is discussed.
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PMID:IN VIVO ANTIVIRAL ACTIVITY OF 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA. 1433 66

A number of nonpolioviruses have been implicated as the probable etiologic agents of paralytic illness clinically resembling poliomyelitis, including certain immunotypes of Coxsackie group A, Coxsackie group B, and ECHO viruses, and the viruses of mumps, herpes simplex and arthropod-borne encephalitides. A number of well documented cases provide evidence that some of these viruses may on occasion be the causative agents of severe, even fatal, myelitis, bulbomyelitis or encephalomyelitis, but they have been associated much more frequently with cases of "poliomyelitis" in which there has been slight to moderate paresis. In the aggregate, various "nonpolioviruses" have been encountered in approximately 10 per cent of the patients with clinical poliomyelitis studied, but it is uncertain how many of these cases may represent coincidental infections not causally related to the current illness.
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PMID:Nonpolioviruses and paralytic disease. 1446 69

Acute hemorrhagic leukoencephalitis (AHLE) is a more severe form of acute disseminated encephalomyelitis (ADEM) characterized by a fulminant clinical course and the presence of hemorrhagic necrosis of the white matter. We report the case of a 57-year-old woman who developed delirium following a respiratory infection. Magnetic resonance imaging of the brain disclosed signal abnormalities in the frontal and temporal lobes, usually found in herpes simplex encephalitis (HSE). Gram stain, India ink and acid-fast bacilli staining were all negative in CSF as was a polymerase chain reaction (PCR) for herpes simplex virus. A diagnosis of AHLE was made and the patient was treated with i.v. methylprednisolone 1g/day for 5 days. Despite treatment, the patient developed several neurological sequelae compatible with the severity of her illness.
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PMID:Acute hemorrhagic leukoencephalitis mimicking herpes simplex encephalitis: case report. 1512 48

Local delivery of cytokines or other immunomodulatory components has been applied as a potential therapy for experimental autoimmune encephalomyelitis (EAE), which is used as a model of human multiple sclerosis. We have used herpes simplex virus-based vectors expressing Th2 cytokines IL-4 and IL-10 and have previously shown a significant abolishment of disease symptoms by the virus expressing IL-4 (R8306), but not by the one expressing IL-10 (R8308). In the present study, the aim was to investigate the local and systemic cytokine response after HSV-based gene therapy. We show that the local expression of IL-4 from an HSV vector delivered to the brain converts the cytokine environment from the disease-promoting Th1-prominent to the disease-limiting IL-4 expressing type. We measured the expression of cytokines IL-4, IL-10, IFN-gamma, IL-12p35, IL-12p40 and the novel IL-23p19 from the brain by quantitative LightCycler RT-PCR. We also investigated the systemic cytokine response from the mouse sera. The results indicate that an increase in the Th2 cytokine IL-4 is observed if the diseased mice are treated with IL-4-expressing virus R8306. Surprisingly, the IL-23 expression of R8306 treated mice was at the same level as in the untreated EAE mice. On the contrary, in the R8308 (IL-10 expression) treated mice, the expression of IL-23 was decreased (P < 0.05). We conclude that the favorable effect of IL-4 on the disease development is more important than the downregulation of the Th1 type cytokines (like IL-23), and that IL-4 would be the key mediator of disease abolishment during gene therapy using these vectors.
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PMID:IL-4 is the key regulator in herpes simplex virus-based gene therapy of BALB/c experimental autoimmune encephalomyelitis. 1519 70

Viral encephalitis, a condition in which a virus infects the brain and produces an inflammatory response, affects approximately 20,000 individuals per year in the United States. The viral encephalidities include sporadic and epidemic acute viral encephalidities and subacute and chronic/progressive viral encephalitis or encephalomyelitis. In people who survive these conditions, postencephalitic impairments of elemental neurologic, cognitive, emotional, and behavioral function are common. This article will provide a brief overview of the diagnosis and acute management of acute viral infections of the central nervous system. The neurologic and neuropsychiatric features, neuropathologies, and treatments of two of the more common types of acute viral encephalitis in North America--herpes simplex encephalitis and West Nile encephalitis--will be reviewed. The current and future role of psychiatrists and neuropsychiatrists in the care and study of individuals with these conditions will be discussed.
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PMID:Viral encephalitis: neuropsychiatric and neurobehavioral aspects. 1535 60

We have previously shown that intracranial infection of herpes simplex virus type 1 (HSV-1) vector R8306 expressing interleukin-4 (IL-4) can abolish symptoms of experimental autoimmune encephalomyelitis, which is used as a model for human multiple sclerosis (Broberg et al., Gene Ther. 8:769-777, 2001). The aim of the current study was to search for means other than intracranial injection to deliver HSV-derived vectors to the central nervous system of mice. We also aimed to study the replication efficiency of these vectors in nervous system tissues and to elucidate the effects of the viruses on the immune response. We studied the spread and replication of the following viruses with deletions in neurovirulence gene gamma(1)34.5: R3616, R849 (lacZ transgene), R3659 (alpha-tk), R8306 (murine IL-4 transgene), and R8308 (murine IL-10 transgene). The samples were taken from trigeminal ganglia and brains of BALB/c mice after corneal, intralabial, and intranasal infection, and the viral load was examined by viral culture, HSV DNA PCR, and VP16 reverse transcription (RT)-PCR. The results show that (i) intranasal infection was the most efficient means of spread to the central nervous system (CNS) besides intracranial injection; (ii) the viruses did not grow in the culture from the brain samples, but the viral DNA persisted even until day 21 postinfection; (iii) viral replication, as observed by VP16 mRNA RT-PCR, occurred mainly on days 4 and 7 postinfection in trigeminal ganglia and to a low extent in brain; (iv) R3659, R8306, and R8308 showed reactivation from the trigeminal ganglia in explant cultures; (v) in the brain, the vectors spread to the midbrain more efficiently than to other brain areas; and (vi) the deletions in the R3659 genome significantly limited the ability of this virus to replicate in the nervous system. The immunological studies show that (i) the only recombinant to induce IL-4 mRNA expression in the brain was R8306, the gamma interferon response was very low in the brain for R3659 and R8306, and the IL-23p19 response to R8306 decreased by day 21 postinfection, unlike for the other viruses; (ii) Deltagamma(1)34.5 HSV vectors modulated the subsets of the splenocytes differently depending on the transgene; (iii) R3659 infection of the nervous system induces expression and production of cytokines from the stimulated splenocytes; and (iv) HSV vectors expressing IL-4 or IL-10 induce expression and production of both of the Th2-type cytokines from splenocytes. We conclude that the intranasal route of infection is a possible means of delivery of Deltagamma(1)34.5 HSV vectors to the CNS in addition to intracranial infection, although replication in the CNS remains minimal. The DNA of the HSV vectors is able to reside in the brain for at least 3 weeks. The features of the immune response to the vectors must be considered and may be exploited in gene therapy experiments with these vectors.
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PMID:Spread and replication of and immune response to gamma134.5-negative herpes simplex virus type 1 vectors in BALB/c mice. 1554 66

The technology of obtaining of specific immunoglobulin for serotherapy of neuroinfection caused by virus herpes simplex 1 type was developed. The patients presented with the following diseases: arachnoencephalitis, encephalopolyradiculoneuritis, encephalomyelitis, encephalitis, arachnoiditis, polyneuropathy, encephalomyelopolyradiculoneuritis, meningoencephalitis. The study showed good tolerance and safety of the medicine, no adverse effects registered during the study. The assessed median score of the efficacy was 2.8 from 3. The obtained results suggest using the liquid form preparation for intramuscular injection "Immunoglobulin for treatment of neuroinfection caused by virus herpes simplex type 1". The Close corporation "Biofarma" located in Kyiv produces this medicine.
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PMID:[Using the preparation "human immunoglobulin against herpes simplex virus type 1 for intramuscular injections" in the complex therapy of nervous system diseases]. 1560 35

Although microglial activation occurs in inflammatory, degenerative and neoplastic central nervous system (CNS) disorders, its role in pathogenesis is unclear. We studied this question by generating CD11b-HSVTK transgenic mice, which express herpes simplex thymidine kinase in macrophages and microglia. Ganciclovir treatment of organotypic brain slice cultures derived from CD11b-HSVTK mice abolished microglial release of nitrite, proinflammatory cytokines and chemokines. Systemic ganciclovir administration to CD11b-HSVTK mice elicited hematopoietic toxicity, which was prevented by transfer of wild-type bone marrow. In bone marrow chimeras, ganciclovir blocked microglial activation in the facial nucleus upon axotomy and repressed the development of experimental autoimmune encephalomyelitis. We conclude that microglial paralysis inhibits the development and maintenance of inflammatory CNS lesions. The microglial compartment thus provides a potential therapeutic target in inflammatory CNS disorders. These results validate CD11b-HSVTK mice as a tool to study the impact of microglial activation on CNS diseases in vivo.
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PMID:Experimental autoimmune encephalomyelitis repressed by microglial paralysis. 1574 34

Acute viral encephalitis may be caused by a wide range of viruses but the most important is herpes simplex encephalitis (HSE) because of its severity, especially if untreated, and its good response to specific treatment with acyclovir. The outcome of any CNS viral infection is dependent on both the immune status of the host and the virulence of the infecting virus. In evaluating a patient with suspected viral encephalitis there are 3 essential steps, namely the identification of a true parenchymal virus infection of the brain rather than a non-infective encephalopathy, the distinction of an infectious viral encephalitis from an acute disseminated encephalomyelitis (ADEM), and then the determination, where possible, of the specific virus involved. In practice, the precise viral cause of the encephalitis may never be established. Analysis of the CSF for herpes simplex virus (HSV) DNA using the Polymerase Chain Reaction (PCR) has been a significant advance in the diagnosis of HSE as this test has a very high sensitivity and specificity especially with appropriate sample timing. It is essential to commence early treatment with intravenous acyclovir in patients suspected of having HSE because of the remarkable safety and efficacy of this drug and the dangers of delaying potentially effective treatment of life threatening disease. This review outlines the general management approach in patients suspected of having viral encephalitis.
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PMID:Viral encephalitis. 1576 75

This article reviews the immunology of the central nervous system and the clinical presentation, diagnosis, and treatment of children with viral or parainfectious encephalitis. The emphasis is on the early recognition of treatable causes of viral encephalitis (herpes simplex virus), and the diagnosis and treatment of acute disseminated encephalomyelitis are described in detail. Laboratory and imaging findings in the two conditions also are described.
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PMID:Pediatric central nervous system infections and inflammatory white matter disease. 1600 59


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