Time course of chemokines in the cerebrospinal fluid and serum during herpes simplex type 1 encephalitis

Rösler, Alexander; Pöhl, Martin; Braune, H.-J.; Oertel, Wolfgang H.; Gemsa, Diethard; Sprenger, Hans

doi:10.1016/s0022-510x(98)00061-6

Cited by 71 publications

(38 citation statements)

References 31 publications

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“…In humans and other vertebrate animals, activated T cells that infiltrate the CNS during encephalitic DNA or RNA viral infections up-regulate expression of the chemokine receptors CCR1, CCR2, CCR5, and CXCR3 and their chemokine ligands CCL2 (CCR2), CCL3 (CCR1, CCR5), CCL4 (CCR5), CCL5 (CCR1, CCR5), and CXCL9 -CXCL11 (CXCR3) (15)(16)(17)(18)(19)(20)(21)(22)(23)(24). Although targeted deletion of CXCR3 or CXCL10 is associated with a reduction in infiltrating mononuclear cells and enhanced mortality from infection of the CNS with mouse hepatitis virus (MHV) 3 (25,26), few studies have examined regional differences in the expression of chemokine ligands during viral encephalitis.…”

Section: T He Infiltration Of Virus-specific Cd8 T Cells Is Essentialmentioning

confidence: 99%

CXCR3 Mediates Region-Specific Antiviral T Cell Trafficking within the Central Nervous System during West Nile Virus Encephalitis

Zhang

Chan

Liu

et al. 2008

The Journal of Immunology

162

147

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Regional differences in inflammation during viral infections of the CNS suggest viruses differentially induce patterns of chemoattractant expression, depending on their cellular targets. Previous studies have shown that expression of the chemokine CXCL10 by West Nile virus (WNV)-infected neurons is essential for the recruitment of CD8 T cells for the purpose of viral clearance within the CNS. In the current study we used mice deficient for the CXCL10 receptor, CXCR3, to evaluate its role in leukocyte-mediated viral clearance of WNV infection within various CNS compartments. WNV-infected CXCR3-deficient mice exhibited significantly enhanced mortality compared with wild-type controls. Immunologic and virologic analyses revealed that CXCR3 was dispensable for control of viral infection in the periphery and in most CNS compartments but, surprisingly, was required for CD8 T cell-mediated antiviral responses specifically within the cerebellum. WNV-specific, CXCR3-expressing T cells preferentially migrated into the cerebellum, and WNV-infected cerebellar granule cell neurons expressed higher levels of CXCL10 compared with similarly infected cortical neurons. These results indicate that WNV differentially induces CXCL10 within neuronal populations and suggest a novel model for nonredundancy in chemokine-mediated inflammation among CNS compartments.

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Section: T He Infiltration Of Virus-specific Cd8 T Cells Is Essentialmentioning

confidence: 99%

CXCR3 Mediates Region-Specific Antiviral T Cell Trafficking within the Central Nervous System during West Nile Virus Encephalitis

Zhang

Chan

Liu

et al. 2008

The Journal of Immunology

162

147

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“…These include interleukin-1␤ (IL-1␤), IL-2, IL-6, IL-10, IL-12, IL-13, tumor necrosis factor alpha (TNF-␣), IFN-␣/␤, IFN-␥, and granulocyte-macrophage colony-stimulating factor (GM-CSF) (69,81,87,94,187,246). In addition, the chemokines IL-8, (207,236). The HSV genome encodes at least 11 glycoproteins, which alone or in concert play different roles in viral adsorption, entry, cell-to-cell spread, immune evasion etc.…”

Section: Herpes Simplex Virusmentioning

confidence: 99%

Molecular Pathways in Virus-Induced Cytokine Production

Mogensen

Paludan

2001

Microbiol Mol Biol Rev

363

324

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Virus infections induce a proinflammatory response including expression of cytokines and chemokines. The subsequent leukocyte recruitment and antiviral effector functions contribute to the first line of defense against viruses. The molecular virus-cell interactions initiating these events have been studied intensively, and it appears that viral surface glycoproteins, double-stranded RNA, and intracellular viral proteins all have the capacity to activate signal transduction pathways leading to the expression of cytokines and chemokines. The signaling pathways activated by viral infections include the major proinflammatory pathways, with the transcription factor NF-κB having received special attention. These transcription factors in turn promote the expression of specific inducible host proteins and participate in the expression of some viral genes. Here we review the current knowledge of virus-induced signal transduction by seven human pathogenic viruses and the most widely used experimental models for viral infections. The molecular mechanisms of virus-induced expression of cytokines and chemokines is also analyzed

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“…Serial changes observed in intrathecal cytokine and chemokine levels in patients with HSE were investigated in 4 separate clinical trials in detail. As a result of these studies; HSE identified in the acute stages of IFN-ү and IL-6 levels increased and these values, confirming the diagnosis has been reported to be helpful (Asaoka et al, 2004;Aurelius et al, 1994;Ichiyama et al, 2008;Rösler et al, 1998). Another preferred method of early diagnosis of HSE is EEG.…”

Section: Serologic Evolutionmentioning

confidence: 64%

Herpes Simplex Type 1 Encephalitis

Sarica¹

2011

Non-Flavivirus Encephalitis

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Time course of chemokines in the cerebrospinal fluid and serum during herpes simplex type 1 encephalitis

Cited by 71 publications

References 31 publications

CXCR3 Mediates Region-Specific Antiviral T Cell Trafficking within the Central Nervous System during West Nile Virus Encephalitis

CXCR3 Mediates Region-Specific Antiviral T Cell Trafficking within the Central Nervous System during West Nile Virus Encephalitis

Molecular Pathways in Virus-Induced Cytokine Production

Herpes Simplex Type 1 Encephalitis

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