Ziegler Thedi, Matikainen Sampsa, Rönkkö Esa, Osterlund Pamela, Sillanpää Maarit, Sirén Jukka, Fagerlund Riku, Immonen Milla, Melén Krister, Julkunen Ilkka
Department of Viral Diseases and Immunology, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland.
J Virol. 2005 Nov;79(21):13800-5. doi: 10.1128/JVI.79.21.13800-13805.2005.
Activation of host innate immune responses was studied in severe acute respiratory syndrome coronavirus (SCV)-infected human A549 lung epithelial cells, macrophages, and dendritic cells (DCs). In all cell types, SCV-specific subgenomic mRNAs were seen, whereas no expression of SCV proteins was found. No induction of cytokine genes (alpha interferon [IFN-alpha], IFN-beta, interleukin-28A/B [IL-28A/B], IL-29, tumor necrosis factor alpha, CCL5, or CXCL10) or IFN-alpha/beta-induced MxA gene was seen in SCV-infected A549 cells, macrophages, or DCs. SCV also failed to induce DC maturation (CD86 expression) or enhance major histocompatibility complex class II expression. Our data strongly suggest that SCV fails to activate host cell cytokine gene expression in human macrophages and DCs.
在严重急性呼吸综合征冠状病毒(SCV)感染的人A549肺上皮细胞、巨噬细胞和树突状细胞(DC)中研究了宿主固有免疫反应的激活情况。在所有细胞类型中,均可见到SCV特异性亚基因组mRNA,但未发现SCV蛋白的表达。在SCV感染的A549细胞、巨噬细胞或DC中,未观察到细胞因子基因(α干扰素[IFN-α]、IFN-β、白细胞介素-28A/B[IL-28A/B]、IL-29、肿瘤坏死因子α、CCL5或CXCL10)或IFN-α/β诱导的MxA基因的诱导。SCV也未能诱导DC成熟(CD86表达)或增强主要组织相容性复合体II类表达。我们的数据强烈表明,SCV无法激活人巨噬细胞和DC中的宿主细胞细胞因子基因表达。