Fig. 1
From: C-type lectins and extracellular vesicles in virus-induced NETosis
Platelets play a central role in virus-induced NET formation and proinflammatory cytokine release. Dengue virus (DV) and immunodeficiency virus type I (HIV-1) interact with DC-SIGN and CLEC2. While DV, LPS, and thrombin can activate platelets to release extracellular vesicles, including exosomes and microvesicles, it is still unclear whether HIV-1 can activate platelets to release EVs. DC-SIGN may associate with CLEC2 to form DC-SIGN/CLEC2 heterocomplex in platelets, thus facilitate platelets to capture various viruses to activate platelets via CLEC2. Platelet-derived exosomes and microvesicles further activate CLEC5A and TLR2, respectively, to enhance DV-induced NET formation and proinflammatory cytokine release. Thus, EVs from activated platelets may serve as common endogenous danger signals to induce NET formation and inflammatory reactions in various microbial infections