Dengue haemorrhagic fever: a job done via exosomes?

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.

Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases

“…Exosomes have shown multi-dimensional roles in DENV life cycle. They can modulate negatively or positively DENV pathogenesis, where they are suggested as instrumental for Dengue Hemorrhagic Fever development in reason of the transportation of specific microRNAs (Mishra et al, 2019). Since HCV can be found inside exosomes (Liu et al, 2014), it is not suprising that blood-derived exosomes from HCV-infected patients can transmit the virus to other cells (Bukong et al, 2014).…”

The Regulation of Flavivirus Infection by Hijacking Exosome-Mediated Cell–Cell Communication: New Insights on Virus–Host Interactions

“…Interestingly, let-7e, mir-1261, mir-371b, and mir-4327 were found in EVs derived from mdDCs infected with the hemorrhagic DENV3-5532 strain, but not in cells infected with the mild DENV3-290 strain (isolated from a mild case of dengue). Thus, these miRNAs could be suitable circulating biomarkers of dengue disease severity, as shown in Figure 4 [ 9 ], as suggested by Mishra et al [ 64 ]. The miRNAs are a type of small non-coding RNA that can regulate gene expression to modulate different biological processes [ 65 ].…”

Neurological Damage by Coronaviruses: A Catastrophe in the Queue!

“…First, viruses were found in the respiratory tract and later were detected in the CNS of susceptible mice, confirming the olfactory route being taken to reach the CNS ( 55 – 58 ). Similarly, murine coronavirus (Mu-CoV) also takes the olfactory nerve route to enter the CNS ( 59 ). The HCoV-OC43 strain is experimentally shown to travel further from the olfactory bulb to other neural regions such as the cortex, hippocampus, and even the brainstem and spinal cord ( 39 ).…”

“…Earlier, many viral infections of HIV-1, Dengue, and other flaviviruses have been reported to cause a cytokine storm phenomenon in the peripheral body which can reach the CNS via either disrupting the BBB or sometime even via trans- cellular crossing of the BBB ( 11 , 72 ). The role of exosomes and other extracellular vesicles in Dengue viral hemorrhagic fever has also been discussed to highlight the importance of exosomal secretion in cytokine storm phenomenon ( 59 ). Even viral proteins such as HIV-1 Tat, Nef, and Dengue NS1 circulate in the bloodstream and trigger the generation and transportation of cytokines to multiple organs, including the CNS ( 73 – 77 ).…”