Abstract
Dengue is an acute febrile disease triggered by dengue virus. Dengue is the widespread and rapidly transmitted mosquito-borne viral disease of humans. Diverse symptoms and diseases due to Dengue virus (DENV) infection ranges from dengue fever, dengue hemorrhagic fever (life-threatening) and dengue shock syndrome characterized by shock, endothelial dysfunction and vascular leakage. Several studies have linked the severity of dengue with the induction of inflammasome. DENV activates the NLRP3-specific inflammasome in DENV infected human patients, mice; specifically, mouse bone marrow derived macrophages (BMDMs), dendritic cells, endothelial cells, human peripheral blood mononuclear cells (PBMCs), keratinocytes, monocyte-differentiated macrophages (THP-1), and platelets. Dengue virus mediated inflammasome initiates the maturation of IL-1β and IL-18, which are critical for dengue pathology and inflammatory response. Several studies have reported the molecular mechanism through which (host and viral factors) dengue induces inflammasome, unravels the possible mechanisms of DENV pathogenesis and sets up the stage for the advancement of DENV therapeutics. In this perspective article, we discuss the potential implications and our understanding of inflammasome mechanisms of dengue virus and highlight research areas that have potential to inhibit the pathogenesis of viral diseases, specifically for dengue.
Highlights
Dengue fever is an acute febrile disease triggered by the dengue virus (DENV)
Dengue virus (DENV) infection comprises immune dysfunction that leads to leakage of vascular fluids and cytokine storm which are suggested as main contributors to the pathogenesis of DENV, culminating in life-threatening hypovolemic shock (Culshaw et al, 2017)
A question arises, whether therapeutics targeting IL-1β may be useful in the treatment of DENV associated diseases? Inflammasome activation plays a crucial role in controlling numerous pathogens, and loss of IL-1β can lead to impaired immune defense
Summary
Dengue fever is an acute febrile disease triggered by the dengue virus (DENV). DENV is positive sense, single stranded, RNA virus, belongs to the Flaviviridae family, genus flavivirus. The study indicated the crucial role that CLEC5A plays in NLRP3 activation, as blockade of CLEC5A blocks the NLRP3 inflammasome activation, and subsequent ablated DENV induced IL-1β production and caspase-1 mediated proptosis in GM-Mφ (Wu et al, 2013b).
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