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Borna disease virus phosphoprotein represses p53-mediated transcriptional activity by interference with HMGB1 Zhang G; Kobayashi T; Kamitani W; Komoto S; Yamashita M; Baba S; Yanai H; Ikuta K; Tomonaga KJ Virol 2003[Nov]; 77 (22): 12243-51Borna disease virus (BDV) is a noncytolytic, neurotropic RNA virus that has a broad host range in warm-blooded animals, probably including humans. Recently, it was demonstrated that a 24-kDa phosphoprotein (P) of BDV directly binds to a multifunctional protein, amphoterin-HMGB1, and inhibits its function in cultured neural cells (W. Kamitani, Y. Shoya, T. Kobayashi, M. Watanabe, B. J. Lee, G. Zhang, K. Tomonaga, and K. Ikuta, J. Virol. 75:8742-8751, 2001). This observation suggested that expression of BDV P may cause deleterious effects in cellular functions by interference with HMGB1. In this study, we further investigated the significance of the binding between P and HMGB1. We demonstrated that P directly binds to the A-box domain on HMGB1, which is also responsible for interaction with a tumor suppression factor, p53. Recent works have demonstrated that binding between HMGB1 and p53 enhances p53-mediated transcriptional activity. Thus, we examined whether BDV P affects the transcriptional activity of p53 by interference with HMGB1. Mammalian two-hybrid analysis revealed that p53 and P competitively interfere with the binding of each protein to HMGB1 in a p53-deficient cell line, NCI-H1299. In addition, P was able to significantly decrease p53-mediated transcriptional activation of the cyclin G promoter. Furthermore, we showed that activation of p21(waf1) expression was repressed in cyclosporine-treated BDV-infected cells, as well as p53-transduced NCI-H1299 cells. These results suggested that BDV P may be a unique inhibitor of p53 activity via binding to HMGB1.|*Transcriptional Activation[MESH]|Animals[MESH]|Binding, Competitive[MESH]|Borna disease virus/*physiology[MESH]|Cell Line, Tumor[MESH]|Cyclin G[MESH]|Cyclin G1[MESH]|Cyclin-Dependent Kinase Inhibitor p21[MESH]|Cyclins/genetics[MESH]|DNA/metabolism[MESH]|HMGB1 Protein/chemistry/*metabolism[MESH]|Rats[MESH]|Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology[MESH]|Viral Proteins/*physiology[MESH] |
