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. 2021 Dec 9;17(12):e1010065.
doi: 10.1371/journal.ppat.1010065. eCollection 2021 Dec.

Insights into potential causes of vascular hyperpermeability in dengue

Andrew Teo  1   2 , Caroline Lin Lin Chua  3 , Po Ying Chia  1   4   5 , Tsin Wen Yeo  1   4   5
Affiliations

Insights into potential causes of vascular hyperpermeability in dengue

Andrew Teo et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interest exist.

Figures

Fig 1
Fig 1. Schematic representation of the EGL and potential EGL disruption during DENV infection.
(A) In a healthy blood vessel, the EGL comprising of complex proteoglycans such as syndecans, HS, and CS can be found on the endothelium. This carbohydrate-rich layer plays an important role in maintaining vascular integrity. (B) In DENV infection, NS-1 triggers the expression and activation of various enzymes that can cleave components within the EGL, leading to loss of EGL integrity and subsequent increased vascular permeability. (C) Other potential mechanisms that link immune cells to increased vascular permeability in DENV infection have also been proposed. Activated neutrophils in dengue patients can release granular proteins such as elastase, myeloperoxidase, and α-defensin 1, which are associated with vascular leakage. NETosis by neutrophils has also been reported in DENV infection; however, the mechanism linking this process to vascular permeability is unknown. Similarly, the activation of MCs leads to degranulation and release of potent mediators such as chymase and tryptase. These proteases were found at increased levels in patients with increased severity of vascular leakage, implying their role in vascular pathology. DENV-activated platelets and EVs released are likely to interact with neutrophils, monocytes, and macrophages, resulting in intensified inflammation that contributes to vascular leakage. In patients with DSS, these mechanisms may be acting in concert to contribute to vascular hyperpermeability. CS, chondroitin sulphate; DENV, dengue virus; DSS, dengue shock syndrome; EGL, endothelial glycocalyx layer; EV, extracellular vesicle; HS, heparan sulphate; IgG, immunoglobulin G; MC, mast cell; MIF, macrophage inhibitory factor; NS-1, nonstructural protein-1.
See this image and copyright information in PMC

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