Padgett R A, Moore D F, Kingsbury D T
J Gen Virol. 1978 Sep;40(3):605-14. doi: 10.1099/0022-1317-40-3-605.
DNA hybridization kinetic analysis of cellular DNA following high multiplicity infection of non-permissive XC cells by herpes simplex virus type I showed that HSV DNA penetrates to the nucleus of the cell but that the number of virus DNA copies present in each cell quickly begins to decline. There did not appear to be any net virus DNA synthesis and the loss of virus DNA copies continued until there was approximately one per haploid genome equivalent. HSV-2 likewise did not show any detectable virus DNA replication. The residual virus information was stable for more than 48 h. CsCl density gradient analysis of the infected cell DNA suggested an association between the HSV DNA and that of the cells. Network analysis also supported the suggestion that a stable association between the virus DNA and host DNA begins shortly after infection. Cell division resulted in the segregation of the virus DNA but not its loss from the cell population. Virus-specific RNA synthesis was easily detectable and 40 to 50% of a labelled DNA probe was converted to an RNA:DNA hybrid.
I型单纯疱疹病毒对非允许性XC细胞进行高感染复数感染后，对细胞DNA进行的DNA杂交动力学分析表明，HSV DNA可穿透到细胞核，但每个细胞中存在的病毒DNA拷贝数很快开始下降。似乎没有任何净病毒DNA合成，病毒DNA拷贝数持续减少，直到每个单倍体基因组当量约有一个拷贝。HSV - 2同样未显示任何可检测到的病毒DNA复制。残留的病毒信息在48小时以上保持稳定。对感染细胞DNA进行的CsCl密度梯度分析表明HSV DNA与细胞DNA之间存在关联。网络分析也支持了病毒DNA与宿主DNA在感染后不久开始形成稳定关联的观点。细胞分裂导致病毒DNA的分离，但并未使其从细胞群体中丢失。病毒特异性RNA合成易于检测，且40%至50%的标记DNA探针转化为RNA:DNA杂交体。
