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. 2018 Nov 8;25:77. doi: 10.1186/s12929-018-0482-9

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Dengue virus interactions with macrophages and endothelial cells that lead to hemorrhage development. a Inoculation by mosquito bite of DENV (DV) into the skin. b The virus infects several cell types including endothelial cells (ECs). c DENV induces production of chemokines that attract macrophages. d DENV stimulates macrophages to produce TNF. e DENV NS2B/3 protease interacts with and cleaves cellular IκBα/IκBβ. DENV NS2B/3 protease also activates IKK, which phosphorylates IκBα and IκBβ. IκBα/IκBβ cleavage enables p50 and p65 translocation into the nucleus, thereby activating NF-κB which results in endothelial cell death. f The presence of TNF in the microenvironment enhances DENV-primed EC apoptosis. Endothelium damage/increased vascular permeability results in hemorrhage development. Solid arrows represent events that enhance endothelium damage. Dotted arrow indicates an event that is speculated to occur [30, 58, 65]