Barker D E, Roizman B
Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, Illinois 60637.
Virology. 1990 Aug;177(2):684-91. doi: 10.1016/0042-6822(90)90534-x.
We report the construction of herpes simplex virus 1 recombinants from which all or part of the coding sequences of four open reading frames have been deleted. In recombinants R7101 and R7108, the BamHI D' fragment containing the coding sequences of the dUTPase gene and the promoter-regulatory domain of a late gene was either replaced with a fragment containing a thymidine kinase gene or deleted, respectively. The recombinant R7107 lacks, in addition to BamHI D', 202 of a total of 244 predicted amino acids from the 3' end of the adjacent open reading frame UL51. The deletion in recombinant R7105 encompasses two genes, i.e., the entire open reading frame of UL47 and the amino terminus of UL46. These genes map next to that specifying the alpha trans-inducing factor. R7105, R7101, and R7108 do not exhibit demonstrable defects in viral replication. The recombinant R7107 forms minute plaques and replicates best in multiplying cells in subconfluent cultures. The results indicate that the multiplying cells supply at least some of the functions expressed by the protein encoded in UL51.
我们报道了单纯疱疹病毒1型重组体的构建,其中四个开放阅读框的全部或部分编码序列已被删除。在重组体R7101和R7108中,包含dUTPase基因编码序列和一个晚期基因启动子调控结构域的BamHI D'片段,分别被一个包含胸苷激酶基因的片段取代或删除。除了BamHI D'之外,重组体R7107还缺少相邻开放阅读框UL51 3'端总共244个预测氨基酸中的202个。重组体R7105中的缺失涵盖两个基因,即UL47的整个开放阅读框和UL46的氨基末端。这些基因与指定α反式诱导因子的基因相邻。R7105、R7101和R7108在病毒复制方面没有表现出明显缺陷。重组体R7107形成微小噬斑,并且在亚汇合培养的增殖细胞中复制最佳。结果表明,增殖细胞至少提供了UL51编码蛋白所表达的一些功能。