Virus Name | Human herpesvirus 4 (Epstein-Barr virus) |
Virus Short Name | EBV |
Order | Herpesvirales |
Virus Family | Herpesviridae |
Virus Subfamily | Gammaherpesvirinae |
Genus | Lymphocryptovirus |
Species | Human herpesvirus 4 |
Host | Human, mammals |
Cell Tropism | B lymphocytes, oral epithelial cells, latency: remains latent in cd19+ b cells |
Associated Disease | Mononucleosis, associated with environemental diseases: burkitt?s lymphoma nasopharyngeal carcinoma (npc) |
Mode of Transmission | Contact, saliva |
VIPR DB link | http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=herpes |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/91/herpesviridae |
Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Herpesviridae |
Paper Title | Neuropilin 1 is an entry factor that promotes EBV infection of nasopharyngeal epithelial cells |
Author's Name | 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 & Mu-Sheng Zeng |
Journal Name | Nature Communications |
Pubmed ID | 25670642 |
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 gB(23-431). 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. |
Used Model | NPEC03,SUNE1, SUNE2, 6-10B, CNE1, CNE2 and HNE1cells |
DOI | 10.1038/ncomms7240 |