Haigh A, Greaves R, O'Hare P
Marie Curie Research Institute, Oxted, Surrey, UK.
Nature. 1990 Mar 15;344(6263):257-9. doi: 10.1038/344257a0.
Induction of transcription of the immediate-early (IE) genes of herpes simplex virus (HSV) involves the assembly of a DNA-binding complex containing the cellular transcription factor Oct-1 and the virus regulatory protein Vmw65 (VP16). Complex assembly can be observed using deletion variants of Vmw65 which lack the acidic C-terminal activation domain and are therefore defective for IE transactivation. Similar variants of Vmw65 interfere with IE activation by the normal protein, and with HSV replication. It has therefore been suggested that dominant interfering products of viruses such as HSV and HIV could be used in a form of intracellular immunization against virus infection. Here we report that a small peptide overlapping a region of Vmw65 which is critical for complex assembly specifically inhibits assembly of the complex but has no observed effect on the DNA-binding activity of the cellular factor alone. Selective interference with the assembly of transcription complexes by short peptides corresponding to functionally critical regions of virus regulatory proteins may be more feasible than the use of defective polypeptides as an antiviral strategy based on competitive interference.
单纯疱疹病毒(HSV)立即早期(IE)基因转录的诱导涉及一种DNA结合复合物的组装,该复合物包含细胞转录因子Oct-1和病毒调节蛋白Vmw65(VP16)。使用缺乏酸性C末端激活域且因此在IE反式激活方面有缺陷的Vmw65缺失变体,可以观察到复合物的组装。Vmw65的类似变体干扰正常蛋白对IE的激活以及HSV的复制。因此有人提出,诸如HSV和HIV等病毒的显性干扰产物可用于一种针对病毒感染的细胞内免疫形式。在此我们报告,一个与Vmw65中对复合物组装至关重要的区域重叠的小肽特异性抑制该复合物的组装,但对单独的细胞因子的DNA结合活性没有观察到影响。基于竞争性干扰,与病毒调节蛋白功能关键区域对应的短肽对转录复合物组装的选择性干扰可能比使用缺陷多肽作为抗病毒策略更可行。