Leung K M, Feng D X, Lou Jianlong, Zhou Yu, Fung K P, Waye Mary M Y, Tsui Stephen K W, Chan Paul K S, Marks James D, Pang S F, Kan Y W
CK Life Sciences International Inc., Hong Kong, SAR, China.
Intervirology. 2008;51(3):173-81. doi: 10.1159/000151530. Epub 2008 Aug 25.
The outbreak of severe acute respiratory syndrome (SARS), caused by a distinct coronavirus, in 2003 greatly threatened public health in China, Southeast Asia as well as North America. Over 1,000 patients died of the SARS virus, representing 10% of infected people. Like other coronaviruses, the SARS virus also utilizes a surface glycoprotein, namely the spike protein, to infect host cells. The spike protein of SARS virus consists of 1,255 amino acid residues and can be divided into two sub-domains, S1 and S2. The S1 domain mediates the binding of the virus to its receptor angiotensin-converting enzyme 2, which is abundantly distributed on the surface of human lung cells. The S2 domain mediates membrane fusion between the virus and the host cell. Hence two strategies can be used to block the infection of the SARS virus, either by interfering with the binding of the S1 domain to the receptor or by blocking the fusion of the virus with the cell membrane mediated by the S2 domain. Several antibodies against the S1 domain have been generated and all of them are able to neutralize the virus in vitro and in vivo using animal models. Unfortunately, point mutations have been identified in the S1 domain, so that the virus isolated in the future may not be recognized by these antibodies. As no mutation has been found in the S2 domain indicating that this region is more conserved than the S1 domain, it may be a better target for antibody binding. After predicting the immunogenicity of the epitopes of the S2 domain, we chemically synthesized two peptides and also expressed one of them using a recombinant DNA method. We screened a phage displaying library of human single-chain antibodies (ScFv) against the predicted epitopes and obtained a human ScFv which can recognize the SARS virus in vitro.
2003年,由一种独特的冠状病毒引起的严重急性呼吸综合征(SARS)疫情,对中国、东南亚以及北美地区的公共卫生构成了严重威胁。超过1000名患者死于SARS病毒,占感染人数的10%。与其他冠状病毒一样,SARS病毒也利用一种表面糖蛋白,即刺突蛋白来感染宿主细胞。SARS病毒的刺突蛋白由1255个氨基酸残基组成,可分为两个亚结构域,S1和S2。S1结构域介导病毒与其受体血管紧张素转换酶2的结合,该受体大量分布在人肺细胞表面。S2结构域介导病毒与宿主细胞之间的膜融合。因此,可以采用两种策略来阻断SARS病毒的感染,要么通过干扰S1结构域与受体的结合,要么通过阻断由S2结构域介导的病毒与细胞膜的融合。已经产生了几种针对S1结构域的抗体,并且所有这些抗体都能够在体外以及使用动物模型在体内中和病毒。不幸的是,在S1结构域中发现了点突变,因此未来分离出的病毒可能无法被这些抗体识别。由于在S2结构域中未发现突变,这表明该区域比S1结构域更保守,它可能是抗体结合的更好靶点。在预测了S2结构域表位的免疫原性之后,我们化学合成了两种肽,并使用重组DNA方法表达了其中一种。我们针对预测的表位筛选了一个展示人单链抗体(ScFv)的噬菌体文库,并获得了一种能够在体外识别SARS病毒的人ScFv。