Role of Complement in Dengue Virus Infection: Protection or Pathogenesis?

Shresta, Sujan

doi:10.1128/mbio.00003-12

Cited by 25 publications

(22 citation statements)

References 18 publications

(23 reference statements)

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“…Complement components inhibit flavivirus infections such as Dengue, West Nile, and Yellow Fever at the replication level or by inducing inflammatory responses which lead to increases in the severity of disease. [52,53] IPA predicted the activation of the complement cascade in our study by 24 hpi. During infection, viral NS1, one of the nonstructural proteins produced after cleavage of the viral polyprotein by host and viral proteases, aids viral pathogenesis by interaction with complement proteins and regulators involved in the complement cascade.…”

Section: Discussionsupporting

confidence: 61%

“…The activation of innate immunity leads to the activation of the complement cascade in response to viral infection. Complement components inhibit flavivirus infections such as Dengue, West Nile, and Yellow Fever at the replication level or by inducing inflammatory responses which lead to increases in the severity of disease . IPA predicted the activation of the complement cascade in our study by 24 hpi.…”

Section: Discussionsupporting

confidence: 49%

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Vero Cell Proteomic Changes Induced by Zika Virus Infection

et al. 2019

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The re‐emergence and the recent spread of the Zika virus (ZIKV) has raised significant global concerns due to lack of information in patient diagnosis and management. Thus, in addition to gaining more basic information about ZIKV biology, appropriate interventions and management strategies are being sought to control ZIKV‐associated diseases and its spread. This study's objective is to identify host cell proteins that are significantly dysregulated during ZIKV infection. SOMAScan, a novel aptamer‐based assay, is used to simultaneously screen >1300 host proteins to detect ZIKV‐induced host protein dysregulation at multiple time points during infection. A total of 125 Vero cell host proteins, including cytokines such as CXCL11 and CCL5, interferon stimulated gene 15, and translation initiation factors EIF5A and EIF4G2, are significantly dysregulated after ZIKV infection. Bioinformatic analyses of 77 host proteins, that are significantly dysregulated ≥1.25‐fold, identify several activated biological processes, including the JAK/STAT, Tec kinase, and complement cascade pathways.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionsupporting

confidence: 49%

Vero Cell Proteomic Changes Induced by Zika Virus Infection

et al. 2019

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“…Factor H is a major regulator of the alternative pathway of the complement system, and abnormal complement responses seem to be involved in dengue pathogenesis [7,11,36]. In our study, we have analyzed the genetic polymorphisms in the promoter and encoding region of CFH gene encoding the human factor H, in a dengue patient cohort.…”

Section: Discussionmentioning

confidence: 99%

Complement factor H gene (CFH) polymorphisms C-257T, G257A and haplotypes are associated with protection against severe dengue phenotype, possible related with high CFH expression

et al. 2013

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Four genetic polymorphisms located at the promoter (C-257T) and coding regions of CFH gene (exon 2 G257A, exon 14 A2089G and exon 19 G2881T) were investigated in 121 dengue patients (DENV-3) in order to assess the relationship between allele/haplotypes variants and clinical outcomes. A statistical value was found between the CFH-257T allele (TT/TC genotypes) and reduced susceptibility to severe dengue (SD). Statistical associations indicate that individuals bearing a T allele presented significantly higher protein levels in plasma. The –257T variant is located within a NF-κB binding site, suggesting that this variant might have effect on the ability of the CFH gene to respond to signals via the NF-κB pathway. The G257A allelic variant showed significant protection against severe dengue. When CFH haplotypes effect was considered, the ancestral CG/CG promoter-exon 2 SNP genotype showed significant risk to SD either in a general comparison (ancestral × all variant genotypes), as well as in individual genotypes comparison (ancestral × each variant genotype), where the most prevalent effect was observed in the CG/CG × CA/TG comparison. These findings support the involvement of –257T, 257A allele variants and haplotypes on severe dengue phenotype protection, related with high basal CFH expression.

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“…13,14 Although many studies have reported that the inflammatory response, cytokine storm, and activation of the complement system play a key role in the progression of severe clinical manifestation, identification of appropriate cytokine profiles, especially during the critical period of illness (defervescence stage) and its association with the progression of severe dengue, is not well established. 8,[15][16][17][18] In this study, we attempted to demonstrate the effects of cytokines in serum of DHF patients by using an in vitro model of HUVEC. Although extensive studies have been conducted during the past several decades, the molecular mechanisms underlying vascular leakage in severe dengue remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Cytokine Factors Present in Dengue Patient Sera Induces Alterations of Junctional Proteins in Human Endothelial Cells

Appanna¹,

Wang²,

Ponnampalavanar³

et al. 2012

The American Journal of Tropical Medicine and Hygiene

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Abstract. Plasma leakage in severe dengue has been postulated to be associated with skewed cytokine immune responses. In this study, the association of cytokines with vascular permeability in dengue patients was investigated. Human serum samples collected from 48 persons (13 with dengue fever, 29 with dengue hemorrhagic fever, and 6 healthy) were subjected to cytokines analysis by using Luminex Multiplex Technology. Selected serum samples from patients with dengue hemorrhagic fever sera and recombinant human cytokines were then tested for roles on inducing vascular permeability by treatment of human umbilical vein endothelial cells. Confocal immunofluorescence staining indicated morphologic alteration of human umbilical vein endothelial cells treated with serum samples from patients with dengue hemorrhagic fever compared with serum samples from healthy persons. The findings suggest that cytokines produced during dengue hemorrhagic infections could induce alterations in the vascular endothelium, which may play a fundamental role in the pathophysiology of dengue.

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Role of Complement in Dengue Virus Infection: Protection or Pathogenesis?

Cited by 25 publications

References 18 publications

Vero Cell Proteomic Changes Induced by Zika Virus Infection

Vero Cell Proteomic Changes Induced by Zika Virus Infection

Complement factor H gene (CFH) polymorphisms C-257T, G257A and haplotypes are associated with protection against severe dengue phenotype, possible related with high CFH expression

Cytokine Factors Present in Dengue Patient Sera Induces Alterations of Junctional Proteins in Human Endothelial Cells

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