Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2. - Wikidata - wikimedia - TriplyDB

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2.

Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2.

http://www.wikidata.org/entity/Q33995740

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Redox Imbalance and Viral Infections in Neurodegenerative Diseases Inhibition of microglia activation as a phenotypic assay in early drug discovery HSV infection induces production of ROS, which potentiate signaling from pattern recognition receptors: role for S-glutathionylation of TRAF3 and 6 Cytomegalovirus-induced sensorineural hearing loss with persistent cochlear inflammation in neonatal mice Prophylactic and therapeutic modulation of innate and adaptive immunity against mucosal infection of herpes simplex virus Modulation of experimental herpes encephalitis-associated neurotoxicity through sulforaphane treatment.Enterovirus 71 induces mitochondrial reactive oxygen species generation that is required for efficient replication.Soybean-derived Bowman-Birk inhibitor inhibits neurotoxicity of LPS-activated macrophages SOCS1/3 expression levels in HSV-1-infected, cytokine-polarized and -unpolarized macrophages Reactive oxygen species drive herpes simplex virus (HSV)-1-induced proinflammatory cytokine production by murine microglia.Evasion of early antiviral responses by herpes simplex viruses.Toll-like receptor 2 mediates peripheral nerve injury-induced NADPH oxidase 2 expression in spinal cord microglia.Neuroprotective Activity of (-)-Epigallocatechin Gallate against Lipopolysaccharide-Mediated Cytotoxicity Pyrrolidine dithiocarbamate inhibits herpes simplex virus 1 and 2 replication, and its activity may be mediated through dysregulation of the ubiquitin-proteasome system.The case for immunomodulatory approaches in treating HSV encephalitis.Elucidation of the block to herpes simplex virus egress in the absence of tegument protein UL16 reveals a novel interaction with VP22.Infectious agents and neurodegeneration.Viral CNS infections: role of glial pattern recognition receptors in neuroinflammation Immune responses to West Nile virus infection in the central nervous system.Innate immune responses in the CNS: role of toll-like receptors, mechanisms, and therapeutic opportunities in multiple sclerosis.Animal models of herpes simplex virus immunity and pathogenesis.Roles of reactive oxygen species in cell signaling pathways and immune responses to viral infections.Reactive oxygen species are induced by Kaposi's sarcoma-associated herpesvirus early during primary infection of endothelial cells to promote virus entry.Herpes simplex virus 1 upregulates p35, alters CDK-5 localization, and stimulates CDK-5 kinase activity during acute infection in neurons.Bovine herpesviruses induce different cell death forms in neuronal and glial-derived tumor cell cultures.Regulated interaction of tegument proteins UL16 and UL11 from herpes simplex virus.TLR2, TLR3, and TLR4 activation specifically alters the oxidative status of intestinal epithelial cells.Involvement of Toll Like Receptor 2 Signaling in Secondary Injury during Experimental Diffuse Axonal Injury in Rats.Protective effect of brown Brazilian propolis against acute vaginal lesions caused by herpes simplex virus type 2 in mice: involvement of antioxidant and anti-inflammatory mechanisms.MCMV triggers ROS/NLRP3-associated inflammasome activation in the inner ear of mice and cultured spiral ganglion neurons, contributing to sensorineural hearing loss.Molecular Mechanisms for Herpes Simplex Virus Type 1 Pathogenesis in Alzheimer's Disease.Vitamin E Supplementation Ameliorates Newcastle Disease Virus-Induced Oxidative Stress and Alleviates Tissue Damage in the Brains of Chickens.Molecular Mechanisms for Herpes Simplex Virus Type 1 Pathogenesis in Alzheimer’s Disease.Induction of Oxidative DNA Damage in Bovine Herpesvirus 1 Infected Bovine Kidney Cells (MDBK Cells) and Human Tumor Cells (A549 Cells and U2OS Cells)

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Herpes simplex virus induces neural oxidative damage via microglial cell Toll-like receptor-2.

http://www.wikidata.org/entity/Q33995740

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Herpes simplex virus induces n ...... ial cell Toll-like receptor-2.

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Journal of Neuroinflammation

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Herpes simplex virus induces n ...... ial cell Toll-like receptor-2.

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P2093

James R Lokensgard

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Morgan R Little

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Scott J Schachtele

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Shuxian Hu

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P2860

Herpes simplex virus type 1 encephalitis is associated with elevated levels of F2-isoprostanes and F4-neuroprostanes

Herpes simplex virus type 1 latency in the murine nervous system is associated with oxidative damage to neurons

Herpes simplex encephalitis: adolescents and adults.

Chronic cortical and subcortical pathology with associated neurological deficits ensuing experimental herpes encephalitis.

Oxidative stress and the pathogenesis of neurodegenerative disorders.

Reactive oxygen species and cell signaling: respiratory burst in macrophage signaling.

Herpes simplex virus 1 interaction with Toll-like receptor 2 contributes to lethal encephalitis.

Toll-like receptors in central nervous system glial inflammation and homeostasis.

Reactive oxygen species and p47phox activation are essential for the Mycobacterium tuberculosis-induced pro-inflammatory response in murine microglia.

Microglia are the major cellular source of inducible nitric oxide synthase during experimental herpes encephalitis

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10.1186/1742-2094-7-35

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7

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Toll-like receptor

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2904293

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