Strayer D S, Laybourn K A, Heard H K
Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, Houston 77030.
Microb Pathog. 1990 Sep;9(3):173-89. doi: 10.1016/0882-4010(90)90020-q.
The relationship of virus-induced immunological dysfunction and tumor dissemination was studied using two related tumor-causing leporipoxviruses: malignant fibroma virus (MV) and Shope fibroma virus (SFV). Recombinant viruses, produced by transferring MV's 10.7 kb BamHI C fragment to SFV, replicate in lymphocytes and suppress lymphocyte function in vitro. Those recombinants that replicate in lymphocytes and suppress lymphocyte function in vitro share about 3.5 kb from MV's C fragment. Some recombinants mimic MV in producing immune suppression and disseminated virus infection in vivo. Other recombinants, even some that are highly immunosuppressive in vitro (e.g. R71), only variably induce immune suppression in vivo, and do not cause disseminated disease. A segment of DNA from MV that transfers to Shope fibroma virus almost all of MV's virulence in vivo was identified.
恶性纤维瘤病毒（MV）和肖普纤维瘤病毒（SFV），研究了病毒诱导的免疫功能障碍与肿瘤播散之间的关系。通过将MV的10.7 kb BamHI C片段转移到SFV而产生的重组病毒，可在淋巴细胞中复制并在体外抑制淋巴细胞功能。那些在淋巴细胞中复制并在体外抑制淋巴细胞功能的重组病毒，从MV的C片段中共享约3.5 kb。一些重组病毒在体内产生免疫抑制和播散性病毒感染方面模仿MV。其他重组病毒，甚至一些在体外具有高度免疫抑制作用的重组病毒（例如R71），在体内仅可变地诱导免疫抑制，并且不会引起播散性疾病。鉴定出一段来自MV的DNA片段，该片段几乎将MV在体内的所有毒力转移给了肖普纤维瘤病毒。
