2. Academic Validation
  3. Function of HAb18G/CD147 in invasion of host cells by severe acute respiratory syndrome coronavirus

Function of HAb18G/CD147 in invasion of host cells by severe acute respiratory syndrome coronavirus

  • J Infect Dis. 2005 Mar 1;191(5):755-60. doi: 10.1086/427811.
Zhinan Chen 1,  Li Mi,  Jing Xu,  Jiyun Yu,  Xianhui Wang,  Jianli Jiang,  Jinliang Xing,  Peng Shang,  Airong Qian,  Yu Li,  Peter X Shaw,  Jianwei Wang,  Shumin Duan,  Jin Ding,  Chunmei Fan,  Yang Zhang,  Yong Yang,  Xiaoling Yu,  Qiang Feng,  Biehu Li,  Xiying Yao,  Zheng Zhang,  Ling Li,  Xiaoping Xue,  Ping Zhu
Affiliations

Affiliation

  • 1 Department of Cell Biology, the Fourth Military Medical University, Xi'an, China.
PMID: 15688292 DOI: 10.1086/427811
Abstract

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.

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