Reed C L, Rapp F
J Virol. 1976 Sep;19(3):1028-33. doi: 10.1128/JVI.19.3.1028-1033.1976.
The interaction of endogenous type C viruses with superinfecting herpes simplex virus type 2 (HSV-2) was investigated in two murine cell lines. Replication of HSV-2 was suboptimal in random-bred Swiss/3T3A cells and, in initial experiments, infection with a low virus-to-cell ratio resulted in carrier cultures with enhanced murine leukemia virus (MuLV) p30 expression. Immunofluorescence tests with Swiss/3T3A cells productively infected with HSV-2 also showed HSV-associated cytoplasmic antigens and enhanced MuLV p30 expression when compared with uninfected controls. Inactivation of HSV-2 with UV light did not abolish this reaction, although the number of cells expressing p30 was reduced. HSV-2 replicated more efficiently in a line of NIH Swiss cells (N c1 A c1 10). These cells are not readily inducible for type C expression by conventional methods; however, untreated and UV-inactivated HSV-2 induced both HSV-2-associated antigens and MuLV p30 in these cells. Although the Birch strain of human cytomegalovirus induced MuLV p30, neither mouse cytomegalovirus nor vesicular stomatitis virus induced MuLV p30 in either cell line.
在两种小鼠细胞系中研究了内源性C型病毒与超感染的单纯疱疹病毒2型（HSV-2）之间的相互作用。在随机繁殖的瑞士/3T3A细胞中，HSV-2的复制不理想，并且在最初的实验中，以低病毒与细胞比例进行感染会导致携带培养物中鼠白血病病毒（MuLV）p30表达增强。与未感染的对照相比，用HSV-2有效感染的瑞士/3T3A细胞进行的免疫荧光测试也显示出与HSV相关的细胞质抗原以及增强的MuLV p30表达。用紫外线使HSV-2失活并没有消除这种反应，尽管表达p30的细胞数量减少了。HSV-2在NIH瑞士细胞系（N c1 A c1 10）中复制更有效。这些细胞不容易通过常规方法诱导C型表达；然而，未处理的和紫外线失活的HSV-2在这些细胞中诱导了HSV-2相关抗原和MuLV p30。虽然人巨细胞病毒的桦树株诱导了MuLV p30，但小鼠巨细胞病毒和水疱性口炎病毒在这两种细胞系中均未诱导MuLV p30。
