Please use this identifier to cite or link to this item: https://doi.org/10.1099/vir.0.055277-0
Title: Dengue virus-infected human monocytes trigger late activation of caspase-1, which mediates pro-inflammatory IL-1 beta secretion and pyroptosis
Authors: Tan, Ter Yong 
Chu, Justin Jang Hann 
Keywords: Apoptosis
Caspase 1
Cells, Cultured
Gene Expression Regulation
Humans
Inflammation
Interleukin-1beta
Monocytes
Time Factors
Transcriptome
Issue Date: Oct-2013
Publisher: Microbiology Society
Citation: Tan, Ter Yong, Chu, Justin Jang Hann (2013-10). Dengue virus-infected human monocytes trigger late activation of caspase-1, which mediates pro-inflammatory IL-1 beta secretion and pyroptosis. JOURNAL OF GENERAL VIROLOGY 94 (PART10) : 2215-2220. ScholarBank@NUS Repository. https://doi.org/10.1099/vir.0.055277-0
Abstract: Dengue virus (DENV) infection affects millions of people annually and has the potential to cause fatal haemorrhagic fever and shock. Although the underlying pathogenesis of severe dengue illness is still unclear, current evidence suggests that severe disease progression has an immunological basis. In this study, we investigated the role of caspase-1 during host-pathogen interactions within DENV-infected human monocytes. Using DENV-infected primary monocytes, we examined caspase-1 at various levels of gene expression and probed for potential immune consequences mediated by caspase-1 such as secretion of pro-inflammatory IL-1β and pyroptotic cell death. We report that DENV-infected monocytes upregulated functional caspase-1 mRNA and pro-caspase-1 activation as a late response to infection. In addition, we found that caspase-1 is responsible for IL-1β secretion and pyroptosis of DENV-infected monocytes. Together, our results show that late caspase-1 activation within DENV-infected monocytes can contribute to pro-inflammatory outcomes that might play a role in dengue immunopathogenesis. © 2013 SGM.
Source Title: JOURNAL OF GENERAL VIROLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/173290
ISSN: 00221317
14652099
DOI: 10.1099/vir.0.055277-0
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