Armstrong M Y, Ruddle N H, Richards F F
J Exp Med. 1977 Apr 1;145(4):1060-5. doi: 10.1084/jem.145.4.1060.
Mice of the low leukemia (BALB/cJ x A/J)F1 hybrid (CAF1) strain express B-and N-tropic infectious murine leukemia virus (MuLV) after the age of 6 mo. Initation of a protracted immunological disorder, the graft-versus-host reaction (GVHR), at 7 wk of age, accelerates the induction of both these mouse-tropic endogenous viruses, and preferentially enhances the replication of B-tropic MuLV. The earlier appearance of B-tropic MuLV in a greater proportion of mice and in higher titer is thought to be casually related to the eventual development of lymphoreticular tumors in the GVHR mice, since previous studies have shown that these same tumors can be reproduced by inoculating syngeneic recipients with serially passaged GVHR extracts containing B-tropic MuLV.
低白血病(BALB/cJ×A/J)F1杂种(CAF1)品系的小鼠在6月龄后表达B型和N型嗜性感染性小鼠白血病病毒(MuLV)。在7周龄时引发持续性免疫紊乱,即移植物抗宿主反应(GVHR),会加速这两种嗜小鼠内源性病毒的诱导,并优先增强B型嗜性MuLV的复制。B型嗜性MuLV在更大比例的小鼠中更早出现且滴度更高,这被认为与GVHR小鼠中淋巴网状肿瘤的最终发生存在因果关系,因为先前的研究表明,通过给同基因受体接种含有B型嗜性MuLV的连续传代GVHR提取物,可以重现这些相同的肿瘤。