Meignier B, Longnecker R, Mavromara-Nazos P, Sears A E, Roizman B
Institut Merieux, Marcy l'Etoile, Charbonnieres les Bains, France.
Virology. 1988 Jan;162(1):251-4. doi: 10.1016/0042-6822(88)90417-5.
We report the results of studies on the biologic properties of seven deletion mutants of herpes simplex virus 1 (HSV-1). The genes deleted from six of these mutants map in the S component of HSV-1 DNA and include those specifying the alpha protein 47, the glycoproteins G and E, the viral protein kinase, and two proteins whose functions are not yet known (open reading frames US2 and US11). The seventh virus [HSV-1(F) delta 305] contained a 700-bp deletion in the thymidine kinase gene. The results of intracerebral inoculation of Balb/c mice indicated that all but one of the deletion mutants in the S component were significantly attenuated. The PFU/LD50 ratios for these mutants ranged from 10(4)- to 10(5)-fold higher than that of the wild-type, HSV-1(F). The PFU/LD50 for mutant R7032, from which the glycoprotein E gene had been deleted, was less than 100-fold higher than that of the parent virus. All of the mutants, with one exception, were able to establish latency in mice; the exception, HSV-1(F) delta 305, was able to establish latency in rabbits.
我们报告了对单纯疱疹病毒1型（HSV-1）七个缺失突变体生物学特性的研究结果。其中六个突变体缺失的基因位于HSV-1 DNA的S组分中，包括编码α蛋白47、糖蛋白G和E、病毒蛋白激酶以及两种功能未知的蛋白（开放阅读框US2和US11）的基因。第七种病毒[HSV-1(F) δ305]在胸苷激酶基因中存在一个700 bp的缺失。对Balb/c小鼠进行脑内接种的结果表明，S组分中的除一个之外的所有缺失突变体均显著减毒。这些突变体的蚀斑形成单位/半数致死剂量（PFU/LD50）比值比野生型HSV-1(F)高10^4至10^5倍。糖蛋白E基因缺失的突变体R7032的PFU/LD50比亲本病毒高不到100倍。除一个例外，所有突变体都能在小鼠中建立潜伏感染；例外的是HSV-1(F) δ305，它能在兔子中建立潜伏感染。
