Vredevoe D L, Hays E F
Cancer Res. 1976 Feb;36(2 Pt 1):370-4.
Virion expression in filtrates of lymphomas in AKR/J or C3H/HeJ mice was assayed by two techniques: (a) in vitro infectivity (XC assay), or (b) acceleration of oncogenicity in vivo (O assay). The two assays appeared to detect different virus populations or activities. This was shown when the same filtrates were tested in parallel by the XC and O tests and opposite results were obtained on the two assays, e.g., XC+ 0- or XC- O+. It was postulated that two viruses, termed "XC+" and "O" to correspond to the assays used to detect them, were involved in oncogenesis. When lymphomas originally virus induced were passaged by cells in 2- to 3-month-old syngeneic AKR or C3H mice, oncogenic activity of filtrates of these transplanted lymphomas decreased as cell passages increased. These filtrates from C3H lymphomas also had decreased XC activity as cell passages increased. Normal lymphoid tissue from 1- to 5-month-old AKR mice was XC+ O-, while from C3H mice it was XC- O-. Thus, the two strains modified activities lacking in their normal tissues. Filtrates highly oncogenic in XC+ newborn AKR mice were oncogenic in C3H newborn mice only when sufficient XC+ virus was in the inoculum received by the XC- C3H mice. Thus the XC+ virus appeared to play a synergistic role with a postulated O virus in oncogenesis.
通过两种技术检测了AKR/J或C3H/HeJ小鼠淋巴瘤滤液中的病毒体表达：(a)体外感染性（XC试验），或(b)体内致癌性加速（O试验）。这两种试验似乎检测到不同的病毒群体或活性。当用XC和O试验对相同的滤液进行平行检测，并在两种试验中得到相反结果时，例如XC+O-或XC-O+，就证明了这一点。据推测，两种病毒参与了肿瘤发生，分别称为“XC+”和“O”，与用于检测它们的试验相对应。当最初由病毒诱导的淋巴瘤在2至3月龄的同基因AKR或C3H小鼠的细胞中传代时，这些移植淋巴瘤滤液的致癌活性随着细胞传代次数的增加而降低。随着细胞传代次数的增加，来自C3H淋巴瘤的这些滤液的XC活性也降低。1至5月龄AKR小鼠的正常淋巴组织为XC+O-，而C3H小鼠的正常淋巴组织为XC-O-。因此，这两个品系改变了其正常组织中所缺乏的活性。在XC+新生AKR小鼠中具有高致癌性的滤液，只有当XC-C3H小鼠接种的接种物中有足够的XC+病毒时，才在C3H新生小鼠中具有致癌性。因此，XC+病毒似乎在肿瘤发生中与一种假定的O病毒起协同作用。
