id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-256582-x2grfhov	Sung, Pei-Shan	CLEC2 and CLEC5A: Pathogenic Host Factors in Acute Viral Infections	2019-12-06		.txt	text/plain	5211	237	35	Moreover, activation of CLEC2 by dengue virus (DV) and H5N1 influenza virus (IAV) induces the release of extracellular vesicles (EVs), which further enhance NETosis and proinflammatory cytokine production via CLEC5A and Toll-like receptor 2 (TLR2). Among these Sykcoupled C-type lectins, activation of CLEC5A by flaviviruses and influenza virus induces the production of inflammatory cytokines and NETosis, while these viruses also activate CLEC2 in platelets to elease extracellular vesicles (EVs), which further enhance inflammatory cytokine release and NETosis via CLEC5A and TLR2 in macrophages and neutrophils. Thus, blockade of CLEC5A-mediated signaling in DV infected cells provides a promising strategy for attenuating systemic vascular leakage and increasing the survival rate of patients suffering from DHF/DSS; this approach might also be applicable to other virus-induced inflammatory diseases (1). These viruses are captured by high affinity receptors (DC-SIGN and MR) to induce inflammatory cytokine release via activation of CLEC5A and CLEC2. Extracellular vesicles from CLEC2-activated platelets enhance dengue virus-induced lethality via CLEC5A/TLR2	./cache/cord-256582-x2grfhov.txt	./txt/cord-256582-x2grfhov.txt