Cell death gene expression profile: Role of RIPK2 in dengue virus-mediated apoptosis

Morchang, Atthapan; Yasamut, Umpa; Netsawang, Janjuree; Noisakran, Sansanee; Wongwiwat, Wiyada; Songprakhon, Pucharee; Srisawat, Chatchawan; Puttikhunt, Chunya; Kasinrerk, Watchara; Malasit, Prida; Yenchitsomanus, Pa Thai; Limjindaporn, Thawornchai

doi:10.1016/j.virusres.2010.12.012

Cited by 32 publications

(21 citation statements)

References 39 publications

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“…Quantitative real-time PCR commercial kits (Search-LC, Roche, Heidelberg, Germany) were used to quantify the expression of genes coding for cytokines: TNF-α, IL-8 and IL-6; apoptosis pathways proteins: BAX, Bcl-2, Bcl-xL and the housekeeping gene PBGD. HRK, PERK, CHOP, PUMA and Noxa were quantified following the real-time PCR protocols described by others, respectively [35]–[37]. The levels of RNA were normalised according to the PBGD mRNA level, which was amplified in duplicate for each of the tested mRNAs using a Bio-Rad CFX96 (Bio-Rad, Hercules, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Crimean-Congo Hemorrhagic Fever Virus-Infected Hepatocytes Induce ER-Stress and Apoptosis Crosstalk

et al. 2012

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Crimean-Congo hemorrhagic fever virus (CCHFV) is a widely distributed tick-borne member of the Nairovirus genus (Bunyaviridae) with a high mortality rate in humans. CCHFV induces a severe disease in infected patients that includes, among other symptoms, massive liver necrosis and failure. The interaction between liver cells and CCHFV is therefore important for understanding the pathogenesis of this disease. Here, we described the in vitro CCHFV-infection and -replication in the hepatocyte cell line, Huh7, and the induced cellular and molecular response modulation. We found that CCHFV was able to infect and replicate to high titres and to induce a cytopathic effect (CPE). We also observed by flow cytometry and real time quantitative RT-PCR evidence of apoptosis, with the participation of the mitochondrial pathway. On the other hand, we showed that the replication of CCHFV in hepatocytes was able to interfere with the death receptor pathway of apoptosis. Furthermore, we found in CCHFV-infected cells the over-expression of PUMA, Noxa and CHOP suggesting the crosstalk between the ER-stress and mitochondrial apoptosis. By ELISA, we observed an increase of IL-8 in response to viral replication; however apoptosis was shown to be independent from IL-8 secretion. When we compared the induced cellular response between CCHFV and DUGV, a mild or non-pathogenic Nairovirus for humans, we found that the most striking difference was the absence of CPE and apoptosis. Despite the XBP1 splicing and PERK gene expression induced by DUGV, no ER-stress and apoptosis crosstalk was observed. Overall, these results suggest that CCHFV is able to induce ER-stress, activate inflammatory mediators and modulate both mitochondrial and death receptor pathways of apoptosis in hepatocyte cells, which may, in part, explain the role of the liver in the pathogenesis of CCHFV.

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Section: Methodsmentioning

confidence: 99%

Crimean-Congo Hemorrhagic Fever Virus-Infected Hepatocytes Induce ER-Stress and Apoptosis Crosstalk

et al. 2012

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“…Death-receptor dependent apoptosis pathway is also implicated in apoptosis of DENV-infected HUVEC cells [88]. The expression of cell death genes including RIPK2, HRK, TGF-beta, PERK, and LC3B during DENV-infection of HepG2 cells is consistent with the activation of apoptosis and autophagy [89]. RIPK2 belongs to the receptor-interacting protein family of serine/threonine protein kinases, which is a crucial mediator of multiple stress responses that leads to the activation of caspase, NF-kappaB, and MAP kinases including JNK and p38.…”

Section: Innate Immune Responsesmentioning

confidence: 99%

The Battle between Infection and Host Immune Responses of Dengue Virus and Its Implication in Dengue Disease Pathogenesis

Sun

Kochel

2013

The Scientific World Journal

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Dengue virus (DENV) is a mosquito-transmitted single stranded RNA virus belonging to genus Flavivirus. The virus is endemic in the tropical and subtropical countries of the world, causing diseases classified according to symptoms and severity (from mild to severe) as dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Among a variety of human cell types targeted by DENV, monocytes, macrophages, and dendritic cells are members of innate immunity, capable of mounting rapid inflammatory responses. These cells are also major antigen presenting cells, responsible for activating the adaptive immunity for long-term memory. This paper is an overview of the current understanding of the following mutually affected aspects: DENV structure, viral infectivity, cellular receptors, innate immune response, and adaptive immunity.

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“…Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a mediator that activates caspases, NF-κB and other kinases. RIPK2 contributes to DENV-mediated apoptosis induced by capsid protein but only for infections involving DENV-2 and -4 serotypes [103]. Additionally, it was recently demonstrated that DENV-3 isolated from a fatal case induces higher rates of apoptosis in monocyte-derived DCs than a strain isolated from a non-fatal case of DF [15].…”

Section: Dengue Virus-induced Apoptosismentioning

confidence: 99%

Dendritic Cell Apoptosis and the Pathogenesis of Dengue

Martins

Silveira

Alves

et al. 2012

Viruses

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Dengue viruses and other members of the Flaviviridae family are emerging human pathogens. Dengue is transmitted to humans by Aedes aegypti female mosquitoes. Following infection through the bite, cells of the hematopoietic lineage, like dendritic cells, are the first targets of dengue virus infection. Dendritic cells (DCs) are key antigen presenting cells, sensing pathogens, processing and presenting the antigens to T lymphocytes, and triggering an adaptive immune response. Infection of DCs by dengue virus may induce apoptosis, impairing their ability to present antigens to T cells, and thereby contributing to dengue pathogenesis. This review focuses on general mechanisms by which dengue virus triggers apoptosis, and possible influence of DC-apoptosis on dengue disease severity.

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Cell death gene expression profile: Role of RIPK2 in dengue virus-mediated apoptosis

Cited by 32 publications

References 39 publications

Crimean-Congo Hemorrhagic Fever Virus-Infected Hepatocytes Induce ER-Stress and Apoptosis Crosstalk

Crimean-Congo Hemorrhagic Fever Virus-Infected Hepatocytes Induce ER-Stress and Apoptosis Crosstalk

The Battle between Infection and Host Immune Responses of Dengue Virus and Its Implication in Dengue Disease Pathogenesis

Dendritic Cell Apoptosis and the Pathogenesis of Dengue

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