Spiegel Martin, Schneider Kerstin, Weber Friedemann, Weidmann Manfred, Hufert Frank T
Institute for Virology, University of Goettingen, Kreuzbergring 57, 37075 Goettingen, Germany.
Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Hermann-Herder-Strasse 11, 79104 Freiburg, Germany.
J Gen Virol. 2006 Jul;87(Pt 7):1953-1960. doi: 10.1099/vir.0.81624-0.
Severe acute respiratory syndrome (SARS) of humans is caused by a novel coronavirus of zoonotic origin termed SARS-associated coronavirus (SARS-CoV). The virus induces severe injury of lung tissue, as well as lymphopenia and destruction of the architecture of lymphatic tissue by as-yet-unknown mechanisms. In this study, the interaction of SARS-CoV with dendritic cells (DCs), the key regulators of immune responses, was analysed. Monocyte-derived DCs were infected with SARS-CoV and analysed for viability, surface-marker expression and alpha interferon (IFN-alpha) induction. SARS-CoV infection was monitored by quantitative RT-PCR, immunofluorescence analysis and recovery experiments. SARS-CoV infected both immature and mature DCs, although replication efficiency was low. Immature DCs were activated by SARS-CoV infection and by UV-inactivated SARS-CoV. Infected DCs were still viable on day 6 post-infection, but major histocompatibility complex class I upregulation was missing, indicating that DC function was impaired. Additionally, SARS-CoV infection induced a delayed activation of IFN-alpha expression. Therefore, it is concluded that SARS-CoV has the ability to circumvent both the innate and the adaptive immune systems.
人类严重急性呼吸综合征（SARS）由一种源自动物的新型冠状病毒即严重急性呼吸综合征相关冠状病毒（SARS-CoV）引起。该病毒通过尚未明确的机制导致肺组织严重损伤，以及淋巴细胞减少和淋巴组织结构破坏。在本研究中，分析了SARS-CoV与免疫反应的关键调节因子树突状细胞（DCs）之间的相互作用。用SARS-CoV感染单核细胞来源的DCs，并分析其活力、表面标志物表达及α干扰素（IFN-α）诱导情况。通过定量逆转录聚合酶链反应、免疫荧光分析和复苏实验监测SARS-CoV感染情况。尽管复制效率较低，但SARS-CoV可感染未成熟和成熟的DCs。未成熟DCs被SARS-CoV感染以及紫外线灭活的SARS-CoV激活。感染的DCs在感染后第6天仍有活力，但主要组织相容性复合体I类分子上调缺失，表明DC功能受损。此外，SARS-CoV感染诱导IFN-α表达延迟激活。因此，得出结论：SARS-CoV有能力规避先天性和适应性免疫系统。
