Author:
Xiong Dan,Du Yong,Wang Hong-Bo,Zhao Bo,Zhang Hua,Li Yan,Hu Li-Juan,Cao Jing-Yan,Zhong Qian,Liu Wan-Li,Li Man-Zhi,Zhu Xiao-Feng,Tsao Sai Wah,Hutt-Fletcher Lindsey M.,Song Erwei,Zeng Yi-Xin,Kieff Elliott,Zeng Mu-Sheng
Abstract
EBV causes B lymphomas and undifferentiated nasopharyngeal carcinoma (NPC). Although the mechanisms by which EBV infects B lymphocytes have been extensively studied, investigation of the mechanisms by which EBV infects nasopharyngeal epithelial cells (NPECs) has only recently been enabled by the successful growth of B lymphoma Mo-MLV insertion region 1 homolog (BMI1)-immortalized NPECs in vitro and the discovery that neuropilin 1 expression positively affects EBV glycoprotein B (gB)-mediated infection and tyrosine kinase activations in enhancing EBV infection of BMI1-immortalized NPECs. We have now found that even though EBV infected NPECs grown as a monolayer at extremely low efficiency (<3%), close to 30% of NPECs grown as sphere-like cells (SLCs) were infected by EBV. We also identified nonmuscle myosin heavy chain IIA (NMHC-IIA) as another NPEC protein important for efficient EBV infection. EBV gH/gL specifically interacted with NMHC-IIA both in vitro and in vivo. NMHC-IIA densely aggregated on the surface of NPEC SLCs and colocalized with EBV. EBV infection of NPEC SLCs was significantly reduced by NMHC-IIA siRNA knock-down. NMHC-IIA antisera also efficiently blocked EBV infection. These data indicate that NMHC-IIA is an important factor for EBV NPEC infection.
Funder
National Basic Research Program of China
China National Fund for Distinguished Young Scientist
National Natural Science Foundation of China
NCI
Publisher
Proceedings of the National Academy of Sciences
Cited by
65 articles.
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