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Enhancement of hepatitis C virus replication by Epstein–Barr virus‐encoded nuclear antigen 1
Author(s) -
Sugawara Yasuhiko,
Makuuchi Masatoshi,
Kato Nobuyuki,
Shimotohno Kunitada,
Takada Kenzo
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.20.5755
Subject(s) - biology , virology , virus , viral replication , antigen , replication (statistics) , hepatitis c virus , hepacivirus , epstein–barr virus , viral transformation , genetics
Based on our recent observation that Epstein–Barr virus (EBV) is detected in 37% of the tissues of hepatocellular carcinoma, and especially frequently in cases with hepatitis C virus (HCV), the effect of EBV infection on the replication of HCV was investigated. EBV‐infected cell clones and their EBV‐uninfected counterparts in cell lines MT‐2 (a human T‐lymphotropic virus type I‐infected T‐cell line), HepG2 (a hepatoblastoma cell line) and Akata (a Burkitt's lymphoma cell line) were compared in terms of their permissiveness for HCV replication following inoculation of HCV derived from patients who were HCV carriers. The results indicated that EBV‐infected cell clones, but not their EBV‐uninfected counterparts, promoted HCV replication. EBV‐encoded nuclear antigen 1 (EBNA1), which is invariably expressed in EBV‐infected cells, supported HCV replication. Deletion analysis of the EBNA1 gene showed good correlation between transactivation activity and the activity supporting HCV replication. The present findings suggest that EBV acts as a helper virus for HCV replication.