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

DSpace/Manakin Repository

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

Citable link to this page

 

 
Title: Neuropilin 1 is an entry factor that promotes EBV infection of nasopharyngeal epithelial cells
Author: Wang, Hong-Bo; Zhang, Hua; Zhang, Jing-Ping; Li, Yan; Zhao, Bo; Feng, Guo-Kai; Du, Yong; Xiong, Dan; Zhong, Qian; Liu, Wan-Li; Du, Huamao; Li, Man-Zhi; Huang, Wen-Lin; Tsao, Sai Wah; Hutt-Fletcher, Lindsey; Zeng, Yi-Xin; Kieff, Elliott; Zeng, Mu-Sheng

Note: Order does not necessarily reflect citation order of authors.

Citation: Wang, H., H. Zhang, J. Zhang, Y. Li, B. Zhao, G. Feng, Y. Du, et al. 2015. “Neuropilin 1 is an entry factor that promotes EBV infection of nasopharyngeal epithelial cells.” Nature Communications 6 (1): 6240. doi:10.1038/ncomms7240. http://dx.doi.org/10.1038/ncomms7240.
Full Text & Related Files:
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.
Published Version: doi:10.1038/ncomms7240
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339892/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:14351058
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters