Fenyö E M, Grundner G, Wiener F, Klein E, Klein G, Harris H
J Exp Med. 1973 May 1;137(5):1240-55. doi: 10.1084/jem.137.5.1240.
The C-type particles produced by the A9 and A9HT sublines of mouse L cells were shown to infect C3H (N type), but not C57BL (B type), mouse embryo fibroblasts. Infection was indicated by distinct single giant cell formation in the XC monolayer used to overlay the mouse embryo fibroblasts. On the basis of these results it was concluded that the L cell virus is N tropic. A9 and A9HT cells were fused to various mouse cells derived from tumors and normal tissues. The ability to produce the Moloney-type surface antigen and to release infectious virus was introduced by the A9 component into the hybrid cell. Virus production, measured by antigen induction on JLS-V9 cells, was suppressed in those hybrids in which the partner cell had a genotype determining low infectibility with that particular virus (B-type cell). It thus appears that the major genetic locus affecting resistance to infection with leukemia viruses, the Fv-1 locus, regulates infectious virus production in somatic cell hybrids also. The same genetic locus did not seem to govern the expression of all virus-related functions, for the virus-determined membrane antigen was demonstrated in many of the N x B-type hybrids in which production of infectious virus was suppressed.
已证明小鼠L细胞的A9和A9HT亚系产生的C型颗粒可感染C3H(N型)小鼠胚胎成纤维细胞,但不能感染C57BL(B型)小鼠胚胎成纤维细胞。用于覆盖小鼠胚胎成纤维细胞的XC单层中形成明显的单个巨细胞表明发生了感染。基于这些结果得出结论,L细胞病毒具有N嗜性。A9和A9HT细胞与源自肿瘤和正常组织的各种小鼠细胞融合。A9成分将产生莫洛尼氏型表面抗原和释放感染性病毒的能力引入杂种细胞。通过对JLS-V9细胞上抗原诱导来测定的病毒产生,在那些其伙伴细胞具有决定对该特定病毒低感染性的基因型(B型细胞)的杂种中受到抑制。因此看来,影响对白血病病毒感染抗性的主要遗传位点,即Fv-1位点,在体细胞杂种中也调节感染性病毒的产生。同一遗传位点似乎并不控制所有与病毒相关功能的表达,因为在许多抑制感染性病毒产生的N×B型杂种中都证明了病毒决定的膜抗原。