汉坦病毒感染致血小板减少的机制  

Mechanism of hantavirus infection causing thrombocytopenia

作　　者：王晓艳 杜虹 李璟 姜泓 申焕君 王平忠 WANG Xiao-yan;DU Hong;LI Jing;JIANG Hong;SHEN Huan-jun;WANG Ping-zhong(Department of Infectious Diseases,the Second Affiliated Hospital of Air Force Medical University,Xi’an 710038,China)

机构地区：[1]空军军医大学第二附属医院传染科,西安710038

出　　处：《传染病信息》2021年第1期83-87,共5页Infectious Disease Information

基　　金：国家自然科学基金面上项目(81373118);陕西省自然科学基金一般项目(2020SF-102)。

摘　　要：汉坦病毒主要感染血管内皮细胞,引起两种人类疾病,即肾综合征出血热和汉坦病毒心肺综合征,它们的共同特点是毛细血管广泛损伤,通透性升高。汉坦病毒感染者血小板数量严重减少,不仅与“外周破坏增加”有关,而且还可能与“血小板生成和功能障碍”有关。尽管汉坦病毒感染引起血小板减少的机制尚不完全明确,但近年也取得了一些重要进展。本文主要围绕血小板减少相关的两种机制展开讨论,旨在阐明汉坦病毒感染发病机制,为治疗肾综合征出血热的药物设计提供指导。Hantavirus mainly infects vascular endothelial cells and causes 2 human diseases,namely hemorrhagic fever with renal syndrome and hantavirus cardiopulmonary syndrome.All hantavirus-associated diseases are characterized by extensive damage to the capillary and increased permeability.In patients infected with hantavirus,there is a dramatic decrease in platelet count,which is associated with“increased peripheral destruction”and also“thrombopoiesis and dysfunction”.Although the mechanism by which hantavirus infection causes thrombocytopenia remains unclear,important advances have been made in recent years.This review focuses on 2 mechanisms related to thrombocytopenia,aiming to clarify the pathogenesis of hantavirus infection and provide guidance for drug design in the treatment of hemorrhagic fever with renal syndrome.

关 键 词：血小板减少 汉坦病毒 肾综合征出血热 

分 类 号：R512.8[医药卫生—内科学]