Viral Bad News Sent by EVAIL.

Viral Bad News Sent by EVAIL.
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DOI:
10.3390/v13061168
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发表时间:
2021-06-18
期刊:
Viruses
影响因子:
--
通讯作者:
Dhillon N
Dhillon N
中科院分区:
其他
文献类型:
--
作者:
Clauss M;Chelvanambi S;Cook C;ElMergawy R;Dhillon N

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本文综述了病毒如何利用细胞外囊泡辅助炎症负荷(EVAIL)发挥病理活动的现有知识。病毒通常被认为是通过急性或慢性感染以及随后的宿主反应来发挥其病理作用。这种宿主反应引起细胞因子的释放,导致血管内皮细胞功能障碍和心血管并发症。然而,病毒可能采用另一种途径来解决可溶性精氨酸诱导的病理学-通过启动细胞外囊泡(EV)的释放,包括外来体。这种替代途径的最好理解的例子是人类免疫缺陷病毒(HIV)引起的EV及其损害血管内皮细胞的倾向。具体而言,一种被称为“负因子”(Nef)的HIV编码的辅助蛋白在来自成功的联合抗逆转录病毒治疗(ART)的HIV患者体液的EV中得到证实;它也被证明足以诱导内皮和心血管功能障碍。本综述将突出HIV-Nef作为HIV如何产生装载促炎货物的EV以传播心血管病变的一个例子。它将进一步讨论EV的产生是否可以解释SARS-CoV-2介导的肺和心血管病理。
This article reviews the current knowledge on how viruses may utilize Extracellular Vesicle Assisted Inflammatory Load (EVAIL) to exert pathologic activities. Viruses are classically considered to exert their pathologic actions through acute or chronic infection followed by the host response. This host response causes the release of cytokines leading to vascular endothelial cell dysfunction and cardiovascular complications. However, viruses may employ an alternative pathway to soluble cytokine-induced pathologies—by initiating the release of extracellular vesicles (EVs), including exosomes. The best-understood example of this alternative pathway is human immunodeficiency virus (HIV)-elicited EVs and their propensity to harm vascular endothelial cells. Specifically, an HIV-encoded accessory protein called the “negative factor” (Nef) was demonstrated in EVs from the body fluids of HIV patients on successful combined antiretroviral therapy (ART); it was also demonstrated to be sufficient in inducing endothelial and cardiovascular dysfunction. This review will highlight HIV-Nef as an example of how HIV can produce EVs loaded with proinflammatory cargo to disseminate cardiovascular pathologies. It will further discuss whether EV production can explain SARS-CoV-2-mediated pulmonary and cardiovascular pathologies.
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