Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Furthermore, excessive NET formation (NETosis) is associated with disease severity in patients suffering from SARS-CoV-2-induced multiple organ injuries. Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and other members of C-type lectin family (L-SIGN, LSECtin, CLEC10A) have been reported to interact with viral glycans to facilitate virus spreading and exacerbates inflammatory reactions. Moreover, spleen tyrosine kinase (Syk)-coupled C-type lectin member 5A (CLEC5A) has been shown as the pattern recognition receptor for members of flaviviruses, and is responsible for DV-induced cytokine storm and Japanese encephalomyelitis virus (JEV)-induced neuronal inflammation. Moreover, DV activates platelets via CLEC2 to release extracellular vesicles (EVs), including microvesicles (MVs) and exosomes (EXOs). The DV-activated EXOs (DV-EXOs) and MVs (DV-MVs) stimulate CLEC5A and Toll-like receptor 2 (TLR2), respectively, to enhance NET formation and inflammatory reactions. Thus, EVs from virus-activated platelets (PLT-EVs) are potent endogenous danger signals, and blockade of C-type lectins is a promising strategy to attenuate virus-induced NETosis and intravascular coagulopathy.

中文翻译：

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病毒诱导的 NETosis 中的 C 型凝集素和细胞外囊泡

在急性病毒感染中观察到中性粒细胞胞外陷阱（NET）形成失调。此外，NETs还有助于急性病毒感染的发病机制，包括由登革热病毒（DV）和严重急性呼吸综合征冠状病毒-2（SARS-CoV-2）引起的感染。此外，过度的 NET 形成 (NETosis) 与 SARS-CoV-2 引起的多器官损伤患者的疾病严重程度相关。据报道，树突状细胞特异性细胞间粘附分子 3 抓取非整合素 (DC-SIGN) 和 C 型凝集素家族的其他成员（L-SIGN、LSECtin、CLEC10A）可与病毒聚糖相互作用，促进病毒传播和加剧炎症反应。此外，脾酪氨酸激酶 (Syk) 偶联的 C 型凝集素成员 5A (CLEC5A) 已被证明是黄病毒成员的模式识别受体，并且负责 DV 诱导的细胞因子风暴和日本脑脊髓炎病毒 (JEV) 诱导的细胞因子风暴。神经元炎症。此外，DV通过CLEC2激活血小板释放细胞外囊泡（EV），包括微泡（MV）和外泌体（EXO）。DV 激活的 EXO (DV-EXO) 和 MV (DV-MV) 分别刺激 CLEC5A 和 Toll 样受体 2 (TLR2)，以增强 NET 形成和炎症反应。因此，来自病毒激活血小板（PLT-EV）的 EV 是有效的内源性危险信号，而阻断 C 型凝集素是减轻病毒诱导的 NETosis 和血管内凝血病的有前途的策略。