Neuropilin 1 is an entry factor that promotes EBV infection of nasopharyngeal epithelial cells

Hong-Bo Wang, Hua Zhang, Jing-Ping Zhang, Yan Li, Bo Zhao, Guo-Kai Feng, Yong Du, Dan Xiong, Qian Zhong, Wan-Li Liu, Huamao Du, Man-Zhi Li, Wen-Lin Huang, Sai Wah Tsao, Lindsey Hutt-Fletcher, Yi-Xin Zeng, Elliott Kieff and Mu-Sheng Zeng ()
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Hong-Bo Wang: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Hua Zhang: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Jing-Ping Zhang: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Yan Li: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Bo Zhao: Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School
Guo-Kai Feng: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Yong Du: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Dan Xiong: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Qian Zhong: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Wan-Li Liu: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Huamao Du: College of Biotechnology, Southwest University
Man-Zhi Li: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Wen-Lin Huang: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Sai Wah Tsao: University of Hong Kong
Lindsey Hutt-Fletcher: Louisiana State University, Health Science Center
Yi-Xin Zeng: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
Elliott Kieff: Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School
Mu-Sheng Zeng: State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract Epstein–Barr virus (EBV) is implicated as an aetiological factor in B lymphomas and nasopharyngeal carcinoma. The mechanisms of cell-free EBV infection of nasopharyngeal epithelial cells remain elusive. EBV glycoprotein B (gB) is the critical fusion protein for infection of both B and epithelial cells, and determines EBV susceptibility of non-B cells. Here we show that neuropilin 1 (NRP1) directly interacts with EBV gB23–431. Either knockdown of NRP1 or pretreatment of EBV with soluble NRP1 suppresses EBV infection. Upregulation of NRP1 by overexpression or EGF treatment enhances EBV infection. However, NRP2, the homologue of NRP1, impairs EBV infection. EBV enters nasopharyngeal epithelial cells through NRP1-facilitated internalization and fusion, and through macropinocytosis and lipid raft-dependent endocytosis. NRP1 partially mediates EBV-activated EGFR/RAS/ERK signalling, and NRP1-dependent receptor tyrosine kinase (RTK) signalling promotes EBV infection. Taken together, NRP1 is identified as an EBV entry factor that cooperatively activates RTK signalling, which subsequently promotes EBV infection in nasopharyngeal epithelial cells.

Date: 2015
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DOI: 10.1038/ncomms7240

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