Chesebro B, Wehrly K, Stimpfling J
J Exp Med. 1974 Dec 1;140(6):1457-67. doi: 10.1084/jem.140.6.1457.
The influence of the major mouse histocompatibility gene complex (H-2) on the response of mice to Friend leukemia virus was studied in F(1) congenic mice differing only at genes within the H-2 complex. F(1) mice which were H-2(b/b) had a high incidence of recovery from splenomegaly compared to H-2(b/d) or H-2(b/a) mice. In mice with recombinations within the H-2 complex a gene (designated RFV-1), responsible for the Friend virus recovery effect, was found to map near or within the D region of serologically detectable transplantation antigens. Because the incidence of recovery was much higher in F(1)H-2(b/b) mice than in parental H-2(b/b) mice, other non-H-2 host genetic factors also appear to be important to expression of recovery in H-2(b/b) F(1) mice. The mechanisms of action of these genes remain unknown.
在仅在H-2复合体内的基因存在差异的F(1)同基因小鼠中，研究了主要小鼠组织相容性基因复合体（H-2）对小鼠对Friend白血病病毒反应的影响。与H-2(b/d)或H-2(b/a)小鼠相比，H-2(b/b)的F(1)小鼠从脾肿大中恢复的发生率较高。在H-2复合体内发生重组的小鼠中，发现一个负责Friend病毒恢复效应的基因（命名为RFV-1）定位在血清学可检测的移植抗原的D区域附近或之内。由于F(1)H-2(b/b)小鼠的恢复发生率远高于亲代H-2(b/b)小鼠，其他非H-2宿主遗传因素似乎对H-2(b/b) F(1)小鼠的恢复表达也很重要。这些基因的作用机制仍然未知。
