Chen D, Stabell E C, Olivo P D
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Virol. 1995 Jul;69(7):4515-8. doi: 10.1128/JVI.69.7.4515-4518.1995.
Varicella-zoster virus (VZV) gene 51 encodes a protein which is homologous to UL9, the origin of DNA replication-binding protein of herpes simplex virus type 1. No genetic information is available on VZV gene 51, but its product has been shown to bind to virtually the same recognition sequence as does UL9 (D. Chen and P. D. Olivo, J. Virol. 68:3841-3849, 1994; N. D. Stow, H. M. Weir, and E. C. Stow, Virology 177:570-577, 1990). We report here that gene 51 can complement a UL9 null mutant (hr94) (A. K. Malik, R. Martinez, L. Muncy, E. P. Carmichael, and S. K. Weller, Virology 190:702-715, 1992), but at a level which is only 20% of that of UL9. Quantitation of viral DNA synthesis suggests that this phenotype is due to a defect in viral DNA synthesis. Regardless, the ability of VZV gene 51 to complement UL9 suggests that alphaherpesviruses have a highly conserved mechanism of initiation of viral DNA synthesis.
水痘带状疱疹病毒(VZV)基因51编码一种与单纯疱疹病毒1型DNA复制起始结合蛋白UL9同源的蛋白质。目前尚无关于VZV基因51的遗传信息,但已证明其产物与UL9结合的识别序列几乎相同(D. Chen和P. D. Olivo,《病毒学杂志》68:3841 - 3849,1994;N. D. Stow、H. M. Weir和E. C. Stow,《病毒学》177:570 - 577,1990)。我们在此报告,基因51可以互补UL9缺失突变体(hr94)(A. K. Malik、R. Martinez、L. Muncy、E. P. Carmichael和S. K. Weller,《病毒学》190:702 - 715,1992),但其水平仅为UL9的20%。病毒DNA合成的定量分析表明,这种表型是由于病毒DNA合成缺陷所致。无论如何,VZV基因51互补UL9的能力表明,α疱疹病毒具有高度保守的病毒DNA合成起始机制。