Nucleocapsid Protein of SARS-CoV Inhibits Cell Cytokinesis and Proliferation by Interacting with Translation Elongation Factor 1

State Key Laboratory of Pathogen and Biosafety, Beijing Institute of Biotechnology, Beijing 100071, China

^* To whom correspondence should be addressed. Email: caoc{at}nic.bmi.ac.cn.

	Abstract

Severe acute respiratory syndrome coronavirus (SARS-CoV) is the etiological agent of severe acute respiratory syndrome, an emerging disease characterized by atypical pneumonia. Using yeast two-hybrid screen with the nucleocapsid (N) protein of SARS-CoV as a bait, the C-terminal (251-422aa) of the N protein was found to interact with human elongation factor 1-alpha (EF1), an essential component of the translational machinery with an important role in cytokinesis by bundling filamentous actin (F-actin). In vitro and in vivo interaction was then confirmed by immuno-coprecipitation, Far-Western blot, and surface plasmon resonance. It was demonstrated that the N protein of SARS-CoV induces aggregation of EF1, inhibiting protein translation and cytokinesis by blocking F-actin bundling. Proliferations of human peripheral blood lymphocytes and other human cell lines were significantly inhibited by the infection of recombinant retrovirus expressing SARS-CoV N protein.