Harland J, Brown S M
J Gen Virol. 1985 Jun;66 ( Pt 6):1305-21. doi: 10.1099/0022-1317-66-6-1305.
We provide evidence that: (i) two variants lacking the XbaI site at map coordinate 0.7 have been selected following XbaI treatment of the DNA of herpes simplex virus type 2 strain HG52; (ii) one of these mutants had lost the 0.7 restriction site due to a deletion of approximately 150 base pairs and in the other the site loss was due to a similar sized sequence insertion; (iii) following XbaI treatment, four variants with deletions ranging in size from 1.5 kb (in both TRL and IRL) to 9 kb in IRL were isolated; (iv) substantial deletions in the long terminal repeat regions of HG52 are present with a frequency of 24% of genomes in the elite stock, a variant with a 3.75 kb deletion in IRL making up 10% and one with a 1.5 kb deletion in both IRL and TRL making up 14%; (v) two of the variants isolated after XbaI treatment of viral DNA were identical to the deletion prototype within the elite stock, suggesting that these variants were not generated as a result of XbaI treatment but pre-existed in the viral DNA pool; (vi) the deletion variants were stably maintained during routine stock propagation, were viable and could be propagated as cloned populations; (vii) the deletions did not have a marked deleterious effect on the one-step growth kinetics of the virus.
（i）在对单纯疱疹病毒2型HG52株的DNA进行XbaI处理后，选择出了两个在图谱坐标0.7处缺乏XbaI位点的变体；（ii）其中一个突变体由于大约150个碱基对的缺失而失去了0.7的限制位点，另一个位点的缺失是由于相似大小的序列插入；（iii）在XbaI处理后，分离出了四个缺失变体，缺失大小从1.5 kb（在TRL和IRL中均有）到IRL中的9 kb不等；（iv）HG52长末端重复区域存在大量缺失，在优良毒株中基因组频率为24%，一个在IRL中有3.75 kb缺失的变体占10%，一个在IRL和TRL中均有1.5 kb缺失的变体占14%；（v）在对病毒DNA进行XbaI处理后分离出的两个变体与优良毒株中的缺失原型相同，这表明这些变体不是XbaI处理产生的，而是预先存在于病毒DNA库中；（vi）缺失变体在常规毒株传代过程中稳定维持，具有活力，并且可以作为克隆群体进行传代；（vii）这些缺失对病毒的一步生长动力学没有明显的有害影响。
