Shao L, Rapp L M, Weller S K
Department of Microbiology, University of Connecticut Health Center, Farmington 06030.
Virology. 1993 Sep;196(1):146-62. doi: 10.1006/viro.1993.1463.
We previously described the isolation of AN-1, a null mutant of the HSV-1 alkaline nuclease gene, which is able to synthesize near wild-type levels of viral DNA and late viral proteins under nonpermissive growth conditions; these results lead us to conclude that the alkaline nuclease is not essential for viral DNA synthesis (Weller, S. K., Seghatoleslami, R. M., Shao, L., Rowse, D., and Carmichael, E. P., 1990, J. Gen. Virol. 71, 2941-2952). AN-1 was found to be deficient in the production of infectious virions suggesting that the nuclease may play a role in processing or packaging of viral DNA into infectious virions. In this report we demonstrate that the defect is distinct from that observed in other late HSV-1 mutants which make but fail to process viral DNA under nonpermissive growth conditions. Following restriction enzyme digestion, specific terminal fragments are observed in DNA from AN-1-infected Vero cells, indicating that specific cleavage has occurred; moreover, the efficiency of cleavage is at near wild-type levels. Also in contrast to cells infected with previously described late mutants, DNase I or staphylococcal nuclease resistant DNA is observed in these cells further indicating that encapsidation has occurred. Three lines of evidence suggest, however, that maturation of DNA-containing AN-1 capsids is defective in some ways. First, in contrast to wild-type, very small amounts of protected DNA is detected in cytoplasmic extracts from AN-1-infected cells. Second, very few if any mature, DNA-containing C capsids are observed in the cytoplasm when analyzed by electron microscopy or sucrose gradient sedimentation. Finally, analysis of nuclei by sucrose gradient sedimentation indicates an elevated ratio of A to B capsids. These data indicate that AN-1 may be defective for the production of capsids competent to mature into the cytoplasm. Possible models for the nature of the defect in AN-1 will be discussed.
我们之前描述了HSV-1碱性核酸酶基因的无效突变体AN-1的分离情况,该突变体在非允许生长条件下能够合成接近野生型水平的病毒DNA和晚期病毒蛋白;这些结果使我们得出结论,碱性核酸酶对于病毒DNA合成并非必不可少(韦勒,S.K.,塞加托莱斯拉米,R.M.,邵,L.,劳斯,D.,以及卡迈克尔,E.P.,1990年,《普通病毒学杂志》71卷,2941 - 2952页)。发现AN-1在感染性病毒粒子的产生方面存在缺陷,这表明核酸酶可能在病毒DNA加工或包装成感染性病毒粒子的过程中发挥作用。在本报告中,我们证明该缺陷与在其他晚期HSV-1突变体中观察到的缺陷不同,那些突变体在非允许生长条件下能够产生但无法加工病毒DNA。经过限制性内切酶消化后,在来自AN-1感染的Vero细胞的DNA中观察到特定的末端片段,这表明发生了特异性切割;此外,切割效率接近野生型水平。同样与感染先前描述的晚期突变体的细胞不同,在这些细胞中观察到了对DNase I或葡萄球菌核酸酶有抗性的DNA,这进一步表明已经发生了衣壳化。然而,有三条证据表明,含有DNA的AN-1衣壳的成熟在某些方面存在缺陷。首先,与野生型相比,在来自AN-1感染细胞的细胞质提取物中检测到的受保护DNA量非常少。其次,通过电子显微镜或蔗糖梯度沉降分析时,在细胞质中观察到的成熟的、含有DNA的C衣壳极少,如果有的话。最后,通过蔗糖梯度沉降对细胞核进行分析表明,A衣壳与B衣壳的比例升高。这些数据表明,AN-1在产生能够成熟进入细胞质的衣壳方面可能存在缺陷。将讨论关于AN-1缺陷性质的可能模型。