Dengue Virus Nonstructural Protein NS5 Induces Interleukin-8 Transcription and Secretion

Medin, Carey L.; Fitzgerald, Katherine A.; Rothman, Alan L.

doi:10.1128/jvi.79.17.11053-11061.2005

Cited by 113 publications

(107 citation statements)

References 72 publications

(76 reference statements)

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“…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

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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

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“…It is therefore likely that DV RNA and/or DV protein(s) are directly involved in the induction of CXCL10/IP-10. For instance, one recent study showed that the DV nonstructural protein NS5 induces CXCL8/IL-8 transcription and secretion (58). Other virus-encoded proteins have also been shown to regulate chemokine expression; the core and NS5A proteins of hepatitis C virus are able to activate the promoter activities of CCL2/MCP-1 and CCL5/RANTES (59); hepatitis C viruses NS5, NS4A, and NS4B induce CXCL8/IL-8 expression (60,61); HIV gp120 induces CXCL10/IP-10 expression (62); and HIV tat regulates CCL2/MCP-1 expression (63).…”

Section: Discussionmentioning

confidence: 99%

Dengue Virus Induces Expression of CXC Chemokine Ligand 10/IFN-γ-Inducible Protein 10, Which Competitively Inhibits Viral Binding to Cell Surface Heparan Sulfate

Chen

Lai

et al. 2006

The Journal of Immunology

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Dengue virus is an arthropod-borne flavivirus that causes a mild febrile illness, dengue fever, or a potentially fatal syndrome, dengue hemorrhagic fever/dengue shock syndrome. Chemokines primarily orchestrate leukocyte recruitment to the areas of viral infection, which makes them critical mediators of immune and inflammatory responses. In the present study, we investigated the induction and function of chemokines in mice early after infection with dengue virus in vivo. We found that CXCL10/IFN-γ-inducible protein 10 (IP-10) expression was rapidly and transiently induced in liver following infection. The expressed CXCL10/IP-10 likely mediates the recruitment of activated NK cells, given that anti-CXCL10/IP-10-treated mice showed diminished NK cell infiltration and reduced hepatic expression of effector molecules in activated NK cells after dengue virus infection. Of particular interest, we found that CXCL10/IP-10 also was able to inhibit viral binding to target cells in vitro. Further investigation revealed that various CXCL10/IP-10 mutants, in which the residues that mediate the interaction between the chemokine and heparan sulfate were substituted, failed to exert the inhibitory effect on dengue binding, which suggests that CXCL10/IP-10 competes with dengue virus for binding to heparan sulfate on the cell surface. Moreover, subsequent plaque assays showed that this inhibition of dengue binding blocked viral uptake and replication. The inhibitory effect of CXCL10/IP-10 on the binding of dengue virus to cells may represent a novel contribution of this chemokine to the host defense against viral infection.

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“…Certain complement fragments such as C3a and C5a are known to enhance permeability. NS1 antigen in dengue virus has been shown to regulate complement activation and hence could play a role in the pathogenesis of DHF [12,13,[25][26][27]. Clearly immunopathogenic mechanisms are involved in plasma leakage and coagulopathy.…”

Section: 2mentioning

confidence: 99%

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

Sellahewa

2013

ISRN Infectious Diseases

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Plasma leakage and intrinsic coagulopathy are the pathological hall marks in dengue haemorrhagic fever (DHF). Viral virulence, infection enhancing antibodies, cytokines and chemical mediators in the setting of intense immune activation are the key players implicated in the pathogenesis of DHF; the exact nature of which is yet to be fully understood. e pathophysiological changes the attended clinical features of plasma leakage necessitate recognition of changing physiological parameters for the early recognition of plasma leakage and appropriate �uid therapy. On the other hand, the changes in the haematological indices resulting from coagulopathy can tempt the clinician to initiate other modalities of therapy. A clearer understanding of the pathogenesis of DHF and the appreciation that both of these fundamental pathological changes share common pathogenic mechanisms would facilitate the appropriateness of management decisions and the early recognition of severe disease. us, thrombocytopaenia, reduced �brinogen, and prolonged partial thromboplastin time early in the disease course connoted severe disease and attended plasma leakage rather than clinical bleeding. e detection of plasma cytokine pro�le by a multiple bead immunoassay could also complement clinical parameters in predicting severe disease early in the disease course. us, MIP-indicates good prognosis while IFN-portends severe disease.

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Dengue Virus Nonstructural Protein NS5 Induces Interleukin-8 Transcription and Secretion

Cited by 113 publications

References 72 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

Dengue Virus Induces Expression of CXC Chemokine Ligand 10/IFN-γ-Inducible Protein 10, Which Competitively Inhibits Viral Binding to Cell Surface Heparan Sulfate

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

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Dengue Virus Nonstructural Protein NS5 Induces Interleukin-8 Transcription and Secretion

Cited by 113 publications

References 72 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

Dengue Virus Induces Expression of CXC Chemokine Ligand 10/IFN-γ-Inducible Protein 10, Which Competitively Inhibits Viral Binding to Cell Surface Heparan Sulfate

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

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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