Function of HAb18G/CD147 in Invasion of Host Cells by Severe Acute Respiratory Syndrome Coronavirus

• Published in: The Journal of infectious diseases Vol. 191; no. 5; pp. 755 - 760
• Main Authors: Chen, Zhinan, Mi, Li, Xu, Jing, Yu, Jiyun, Wang, Xianhui, Jiang, Jianli, Xing, Jinliang, Shang, Peng, Qian, Airong, Li, Yu, Shaw, Peter X., Wang, Jianwei, Duan, Shumin, Ding, Jin, Fan, Chunmei, Zhang, Yang, Yang, Yong, Yu, Xiaoling, Feng, Qiang, Li, Biehu, Yao, Xiying, Zhang, Zheng, Li, Ling, Xue, Xiaoping, Zhu, Ping
• Format: Journal Article
• Language: English
• Published: United States The University of Chicago Press 01.03.2005; Oxford University Press
• Subjects: Antigens, CD - physiology; Basigin; Cell Line; Coronavirus Nucleocapsid Proteins; Cyclophilin A - physiology; Cytopathogenic Effect, Viral - physiology; Gene Expression; Humans; Major and Brief Reports; Nucleocapsid Proteins - physiology; Protein Binding; SARS coronavirus; Severe acute respiratory syndrome-related coronavirus - pathogenicity; Viral Structural Proteins - physiology
• ISSN: 0022-1899; 1537-6613; 1537-6613
• DOI: 10.1086/427811

To identify the function of HAb18G/CD147 in invasion of host cells by severe acute respiratory syndrome (SARS) coronavirus (CoV), we analyzed the protein-protein interaction among HAb18G/CD147, cyclophilin A (CyPA), and SARS-CoV structural proteins by coimmunoprecipitation and surface plasmon resonance analysis. Although none of the SARS-CoV proteins was found to be directly bound to HAb18G/CD147, the nucleocapsid (N) protein of SARS-CoV was bound to CyPA, which interacted with HAb18G/CD147. Further research showed that HAb18G/CD147, a transmembrane molecule, was highly expressed on 293 cells and that CyPA was integrated with SARS-CoV. HAb18G/CD147–antagonistic peptide (AP)–9, an AP of HAb18G/CD147, had a high rate of binding to 293 cells and an inhibitory effect on SARS-CoV. These results show that HAb18G/CD147, mediated by CyPA bound to SARS-CoV N protein, plays a functional role in facilitating invasion of host cells by SARS-CoV. Our findings provide some evidence for the cytologic mechanism of invasion by SARS-CoV and provide a molecular basis for screening anti-SARS drugs