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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Res 2015 ; 25 (7): 785-800 Nephropedia Template TP
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In-cell infection: a novel pathway for Epstein-Barr virus infection mediated by cell-in-cell structures #MMPMID25916549
Ni C; Chen Y; Zeng M; Pei R; Du Y; Tang L; Wang M; Hu Y; Zhu H; He M; Wei X; Wang S; Ning X; Wang M; Wang J; Ma L; Chen X; Sun Q; Tang H; Wang Y; Wang X
Cell Res 2015[Jul]; 25 (7): 785-800 PMID25916549show ga
Epstein-Barr virus (EBV) can infect both susceptible B lymphocytes and non-susceptible epithelial cells (ECs). Viral tropism analyses have revealed two intriguing means of EBV infection, either by a receptor-mediated infection of B cells or by a cell-to-cell contact-mediated infection of non-susceptible ECs. Herein, we report a novel ?in-cell infection? mechanism for EBV infection of non-susceptible ECs through the formation of cell-in-cell structures. Epithelial CNE-2 cells were invaded by EBV-infected Akata B cells to form cell-in-cell structures in vitro. Such unique cellular structures could be readily observed in the specimens of nasopharyngeal carcinoma. Importantly, the formation of cell-in-cell structures led to the autonomous activation of EBV within Akata cells and subsequent viral transmission to CNE-2 cells, as evidenced by the expression of viral genes and the presence of virion particles in CNE-2 cells. Significantly, EBV generated from in-cell infected ECs displayed altered tropism with higher infection efficacy to both B cells and ECs. In addition to CNE-2 tumor cells, cell-in-cell structure formation could also mediate EBV infection of NPEC1-Bmi1 cells, an immortalized nasopharyngeal epithelial cell line. Furthermore, efficient infection by this mechanism involved the activation of the PI3K/AKT signaling pathway. Thus, our study identified ?in-cell infection? as a novel mechanism for EBV infection. Given the diversity of virus-infected cells and the prevalence of cell-in-cell structures during chronic infection, we speculate that ?in-cell infection? is likely a general mechanism for EBV and other viruses to infect non-susceptible ECs.