严重急性呼吸综合征冠状病毒的3a蛋白可诱导非洲绿猴肾细胞系E6细胞凋亡。

The 3a Protein of SARS-coronavirus Induces Apoptosis in Vero E6 Cells.

作者信息

Y Waye Mary, W Law Patrick, Wong Chi-Hang, C Au Thomas, Chuck Chi-Pang, Kong Siu-Kai, S Chan Paul, To Ka-Fai, I Lo Anthony, W Chan Judy, Suen Yick-Keung, Edwin Chan H Y, Fung Kwok-Pui, Y Sung Joseph, Lo Y M, W Tsui Stephen

机构信息

Department of Biochemistry, The Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China.

出版信息

Conf Proc IEEE Eng Med Biol Soc. 2005;2005:7482-5. doi: 10.1109/IEMBS.2005.1616242.

DOI:10.1109/IEMBS.2005.1616242

PMID:17282011

Abstract

An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid November 2002. The etiologic agent of this disease was found to be a previously unknown coronavirus, SARS-CoV. The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein which is predicted to be a transmembrane protein. In this study, we showed that the 3a protein was localized to the endoplasmic reticulum (ER) in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggest that the 3a protein may trigger apoptosis. Our data show that over-expression of a single SARS-CoV protein can induce apoptosis in vitro. Thus GFP-3a fusion protein could also be used as a biosensor for monitoring the cytopathic features of SARS infection, e.g. lymphopenia, in animal model systems, similar to nucleocapsid and 7a proteins.

摘要

严重急性呼吸综合征（SARS）疫情在中国爆发，首例病例于2002年11月中旬出现。该疾病的病原体被发现是一种此前未知的冠状病毒，即SARS-CoV。SARS-CoV感染的详细病理学以及宿主对病毒感染的反应仍不清楚。3a基因编码一种非结构病毒蛋白，预计为跨膜蛋白。在本研究中，我们发现3a蛋白在转染了3a的猴肾Vero E6细胞中定位于内质网（ER）。染色质浓缩和DNA片段化的体外实验表明，3a蛋白可能触发细胞凋亡。我们的数据表明，单一SARS-CoV蛋白的过表达可在体外诱导细胞凋亡。因此，GFP-3a融合蛋白也可作为生物传感器，用于监测动物模型系统中SARS感染的细胞病变特征，如淋巴细胞减少，类似于核衣壳蛋白和7a蛋白。