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严重急性呼吸综合征的发病机制

Pathogenesis of severe acute respiratory syndrome.

作者信息

Lau Yu Lung, Peiris J S Malik

机构信息

Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Room 117 New Clinical Building, Queen Mary Hospital, Pokfulam Road, Hong Kong.

出版信息

Curr Opin Immunol. 2005 Aug;17(4):404-10. doi: 10.1016/j.coi.2005.05.009.

DOI:10.1016/j.coi.2005.05.009
PMID:15950449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7127490/
Abstract

Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441-700 of the spike protein (S protein) as the major epitope.

摘要

严重急性呼吸系统综合征(SARS)是一种由新型冠状病毒(CoV)引起的人畜共患传染病。SARS-CoV的组织嗜性不仅包括肺,还包括胃肠道、肾脏和肝脏。血管紧张素转换酶2(ACE2)、C型凝集素CD209L(也称为L-SIGN)和DC-SIGN可结合SARS-CoV,但ACE2似乎是该病毒的关键功能性受体。对SARS-CoV感染存在显著的先天性免疫反应,包括急性期蛋白、趋化因子、炎性细胞因子和C型凝集素,如甘露糖结合凝集素,其对SARS起保护作用。相比之下,可能缺乏1型干扰素反应。此外,急性期常见淋巴细胞减少,CD4+和CD8+T细胞数量减少。康复患者具有IgG类中和抗体,可识别刺突蛋白(S蛋白)441-700位氨基酸作为主要表位。

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