The amino acid region 248-382 of the Epstein-Barr virus nuclear protein 2 (EBNA2) is responsible for the EBNA2-induced EBV reactivation.
We showed previously that Epstein-Barr virus (EBV) latency is disrupted and the virus-replicative cycle is activated after expression of EBNA2 in the Burkitt's lymphoma-derived Akata cells. Here, an EBNA2 deletion mutant lacking the amino acid residues 248-382, including the region responsible for association with RBP-J kappa, was generated and tested for its ability to activate EBV replication in Akata cells. This mutant was shown clearly deficient in inducing the EBV-replicative cycle, suggesting that association with RBP-J kappa is necessary for the EBV activating function of EBNA2. It is thus likely that EBV activation by EBNA2, seemingly in conflict with its involvement in lymphocyte immortalization, is nevertheless based on the standard mechanism of transactivation by the protein.
Fujiwara
S
S
Department of Immunology and Microbiology, Nihon University School of Medicine, Tokyo, Japan. shige@med.nihon-u.ac.jp
Liu
E
E
Shimizu
K
K
D002460:Cell Line; D019309:Epstein-Barr Virus Nuclear Antigens / Q000235:genetics* / Q000502:physiology; D004854:Herpesvirus 4, Human / Q000235:genetics* / Q000502:physiology; D017434:Protein Structure, Tertiary / Q000235:genetics / Q000502:physiology; D014764:Viral Proteins; D014775:Virus Activation / Q000502:physiology
C402641:EBNA-2 protein, Human herpesvirus 4; D019309:Epstein-Barr Virus Nuclear Antigens; D014764:Viral Proteins