Upregulation of RANTES Gene Expression in Neuroglia by Japanese Encephalitis Virus Infection

Chen, Chun‐Jung; Chen, Jianhong; Chen, Shih‐Yun; Liao, Su‐Lan; Raung, Shue-Ling

doi:10.1128/jvi.78.22.12107-12119.2004

Cited by 122 publications

(90 citation statements)

References 82 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although measles viruses has been shown to inhibit HIV replication independent of chemokines in vitro (46), several members of the Flavivirus family (HCV, Japanese Encephalitis Virus and Dengue Virus) alter the cellular release of cytokines and chemokines (47)(48)(49). Thus, chemokine and cytokine modulation may be a common feature of Flavivirus replication, and the effects observed with GBV-C NS5A protein may be found in related viruses as well.…”

Section: Discussionmentioning

confidence: 99%

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

Xiang

McLinden

Chang

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

115

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

Xiang

McLinden

Chang

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

115

View full text Add to dashboard Cite

show abstract

“…T, B cells, and macrophages [72]. In vitro work has demonstrated that microglia and astrocytes are the main cells that produce CCL5 during JEV infection [84]. In mice, microarray analysis shows an upregulation of CCL5 in the brain of JEV-infected mice [83,85].…”

Section: Ccl5mentioning

confidence: 99%

The role of chemokines in the pathogenesis of neurotropic flaviviruses

Bardina

Lim

2012

Immunol Res

View full text Add to dashboard Cite

Neurotropic flaviviruses are important emerging and reemerging arthropod-borne pathogens that cause significant morbidity and mortality in humans and other vertebrates worldwide. Upon entry and infection of the CNS, these viruses can induce a rapid inflammatory response characterized by the infiltration of leukocytes into the brain parenchyma. Chemokines and their receptors are involved in coordinating complex leukocyte trafficking patterns that regulate viral pathogenesis in vivo. In this review, we will summarize the current literature on the role of chemokines in regulating the pathogenesis of West Nile, Japanese encephalitis, and tick-borne encephalitis virus infections in mouse models and humans. Understanding how viral infections trigger chemokines, the key cellular events that occur during the infection process, as well as the immunopathogenic role of these cells, are critical areas of research that may ultimately guide a much needed effort toward developing specific immunomodulators and/or antiviral therapeutics.

show abstract

“…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

164

147

View full text Add to dashboard Cite

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.

show abstract

Upregulation of RANTES Gene Expression in Neuroglia by Japanese Encephalitis Virus Infection

Cited by 122 publications

References 82 publications

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

The role of chemokines in the pathogenesis of neurotropic flaviviruses

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

Contact Info

Product

Resources

About

Upregulation of RANTES Gene Expression in Neuroglia by Japanese Encephalitis Virus Infection

Cited by 122 publications

References 82 publications

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 + Jurkat T cells

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 + Jurkat T cells

The role of chemokines in the pathogenesis of neurotropic flaviviruses

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

Contact Info

Product

Resources

About

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells

An 85-aa segment of the GB virus type C NS5A phosphoprotein inhibits HIV-1 replication in CD4 ⁺ Jurkat T cells