SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.
SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.
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DOI：
10.1016/j.coviro.2012.04.004
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发表时间：
2012-06
影响因子：
5.9
通讯作者：
Baric RS
中科院分区：
文献类型：
--
作者：
Totura AL;Baric RS
SARS-CoV感染的细胞培养、小鼠和非人灵长类动物模型已被开发用于先天免疫发病机制的研究。SARS-CoV先天免疫感应的宿主机制尚不清楚，但有证据表明参与了RLR和TLR。异常的促炎细胞因子和干扰素刺激的基因反应与严重SARS-CoV疾病的表型相关。SARS-CoV蛋白质调节先天免疫反应，拮抗干扰素反应，避免宿主传感机制的检测。SARS-CoV是一种致病性冠状病毒，来自人畜共患病宿主，导致病毒在全球传播。SARS-CoV与患者异常细胞因子、趋化因子和干扰素刺激基因（ISG）反应的关联提供了证据，表明SARS-CoV的发病机制至少部分受到先天免疫信号传导的控制。利用SARS-CoV感染模型，先天免疫信号通路的关键组分已被确定为抗SARS-CoV疾病的保护因子，包括STAT 1和MyD 88。SARS-CoV疾病状态下特有的基因转录特征已被鉴定，但调节加重疾病表型的宿主因素仍在很大程度上未确定。SARS-CoV编码的几种蛋白通过拮抗干扰素的诱导和避免ISG效应子功能来调节先天免疫信号传导。
► Robust cell culture, mouse, and nonhuman primate models of SARS-CoV infection have been developed for the study of innate immune pathogenesis. ► Host mechanisms of innate immune sensing of SARS-CoV are unknown, but there is evidence for the involvement of RLRs and TLRs. ► Aberrant proinflammatory cytokine and Interferon Stimulated Gene responses are associated with phenotypes of severe SARS-CoV disease. ► SARS-CoV proteins that modulate innate immune responses antagonize the Interferon response and avoid detection by host sensing mechanisms. SARS-CoV is a pathogenic coronavirus that emerged from a zoonotic reservoir, leading to global dissemination of the virus. The association SARS-CoV with aberrant cytokine, chemokine, and Interferon Stimulated Gene (ISG) responses in patients provided evidence that SARS-CoV pathogenesis is at least partially controlled by innate immune signaling. Utilizing models for SARS-CoV infection, key components of innate immune signaling pathways have been identified as protective factors against SARS-CoV disease, including STAT1 and MyD88. Gene transcription signatures unique to SARS-CoV disease states have been identified, but host factors that regulate exacerbated disease phenotypes still remain largely undetermined. SARS-CoV encodes several proteins that modulate innate immune signaling through the antagonism of the induction of Interferon and by avoidance of ISG effector functions.
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DOI：
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