Zalani S, Coppage A, Holley-Guthrie E, Kenney S
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, 27599-7295, USA.
J Virol. 1997 Apr;71(4):3268-74. doi: 10.1128/JVI.71.4.3268-3274.1997.
Disruption of Epstein-Barr virus latency is induced by expression of either the BZLF1 (in B cells and epithelial cells) or BRLF1 (in epithelial cells only) immediate-early protein. Regulation of BZLF1 and BRLF1 transcription may therefore modulate the stringency of viral latency. The cellular transcription factor YY1 negatively regulates BZLF1 transcription. Here we show that the BRLF1 promoter (Rp) sequences from -206 to -227 (relative to the mRNA start site) and from -7 to +6 are directly bound by YY1. Mutation of the upstream YY1 binding site increases constitutive Rp activity in epithelial cells and B cells, while mutation of the downstream YY1 binding site does not significantly affect Rp activity. Negative regulation of BZLF1 and BRLF1 transcription by YY1 may act to maintain viral latency.
爱泼斯坦-巴尔病毒潜伏期的破坏是由BZLF1(在B细胞和上皮细胞中)或BRLF1(仅在上皮细胞中)立即早期蛋白的表达所诱导的。因此,BZLF1和BRLF1转录的调节可能会调节病毒潜伏期的严格程度。细胞转录因子YY1负向调节BZLF1转录。在这里,我们表明,YY1直接结合BRLF1启动子(Rp)从-206到-227(相对于mRNA起始位点)以及从-7到+6的序列。上游YY1结合位点的突变增加了上皮细胞和B细胞中组成型Rp活性,而下游YY1结合位点的突变对Rp活性没有显著影响。YY1对BZLF1和BRLF1转录的负向调节可能起到维持病毒潜伏期的作用。