Abstract
ABSTRACT Dengue fever is one of those unique diseases where host immune responses largely determine the pathogenesis and its severity. Earlier studies have established the fact that dengue virus (DENV) infection causes haemorrhagic fever and shock syndrome, but it is not directly responsible for exhibiting these clinical symptoms. It is noteworthy that clinically, vascular leakage syndrome does not develop for several days after infection despite a robust innate immune response that elicits the production of proinflammatory and proangiogenic cytokines. The onset of hyperpermeability in severe cases of dengue disease takes place around the time of defervescence and after clearance of viraemia. Extracellular vesicles are known to carry biological information (mRNA, miRNA, transcription factors) from their cells of origin and have emerged as a significant vehicle for horizontal transfer of stress signals. In dengue virus infection, the relevance of exosomes can be instrumental since the majority of the immune responses in severe dengue involve heavy secretion and circulation of pro-inflammatory cytokines and chemokines. Here, we present an updated review which will address the unique and puzzling features of hyperpermeability associated with DENV infection with a special focus on the role of secreted extracellular vesicles.
Highlights
Dengue fever is caused by the infection of dengue virus
We have attempted to highlight the notion that a single theory of Dengue Haemorrhagic Fever (DHF) cannot explain the whole scenario alone
DHF is a phenomenon which occurs at multiple places in the host despite the fact that dengue virus (DENV) is not homogenously distributed either temporally or spatially
Summary
Dengue fever is caused by the infection of dengue virus. It is a mosquito-born disease identified just 100 years ago [1]. Many reports of dengue haemorrhagic fever in the primary infection ( lesser extent) indicate that antibody-dependent enhancement is not an essential pre-requisite for plasma leakage [1]. These findings strongly suggest that elevated viral load due to ADE alone is not the direct cause of vascular leakage and probably other mechanisms play an important role in triggering and contributing towards DHF phenomenon.
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