Establishment and characterization of a novel Hodgkin lymphoma cell line, AM-HLH, carrying the Epstein-Barr virus genome integrated into the host chromosome

2016 ◽  
Vol 35 (4) ◽  
pp. 567-575 ◽  
Author(s):  
Masahiko Hayashida ◽  
Masanori Daibata ◽  
Erika Tagami ◽  
Takahiro Taguchi ◽  
Fumiyo Maekawa ◽  
...  
1988 ◽  
Vol 156 (4) ◽  
pp. 319-330 ◽  
Author(s):  
YOSHIHIRO NOZAWA ◽  
MASAFUMI ABE ◽  
HARUKI WAKASA ◽  
HITOSHI OHNO ◽  
SHIROU FUKUHARA ◽  
...  

2009 ◽  
Vol 84 (6) ◽  
pp. 2893-2901 ◽  
Author(s):  
Ami Watanabe ◽  
Seiji Maruo ◽  
Taku Ito ◽  
Miho Ito ◽  
Koichi Ricardo Katsumura ◽  
...  

ABSTRACT Burkitt lymphoma (BL) is etiologically associated with Epstein-Barr virus (EBV). EBV-positive BL tumors display two latent forms of infection. One is referred to as latency I infection, in which EBV expresses the virus genome maintenance protein EBNA1 as the only viral protein. The other is referred to as Wp-restricted latency and was recently identified in a subset of BL tumors. In these tumors, EBV expresses EBNA1, EBNA3A, EBNA3B, EBNA3C, a truncated form of EBNA-LP, and the viral Bcl-2 homologue BHRF1, all of which are driven by the BamHI W promoter (Wp). To investigate the role of EBV in Wp-restricted BL, we conditionally expressed a dominant-negative EBNA1 (dnEBNA1) mutant which interrupts the virus genome maintenance function of EBNA1 in the P3HR-1 BL cell line. Induction of dnEBNA1 expression caused loss of the EBV genome and resulted in apoptosis of P3HR-1 cells in the absence of exogenous apoptosis inducers, indicating that P3HR-1 cells cannot survive without EBV. Stable transfection of the BHRF1 gene into P3HR-1 cells rescued the cells from the apoptosis induced by dnEBNA1 expression, whereas stable transfection of truncated EBNA-LP, EBNA3A, or EBNA3C did not. Moreover, knockdown of BHRF1 expression in P3HR-1 cells resulted in increased cell death. These results indicate that EBV is essential for the survival of P3HR-1 cells and that BHRF1 functions as a survival factor. Our finding implies a critical contribution of BHRF1 to the pathogenesis of Wp-restricted BLs.


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