Dietz M, Fouchey S P, Longley C, Rich M A, Furmanski P
Department of Biology, Michigan Cancer Foundation, Detroit 48201.
J Exp Med. 1977 Mar 1;145(3):594-606. doi: 10.1084/jem.145.3.594.
The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV-RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV is N-tropic. Passage of nonregressing CFV through Fv-1 incompatible Swiss/ICR mice changed the tropism of CFV from N to NB and resulted in a virus strain which induced erythroleukemia that regressed. Passage of NB-tropic CFV back through Fv-1 compatible mice maintained NB-tropism and regression. Altering the quantity or type of helper MuLV in RFV complex by addition of Ri-MuLV inhibited regression in proportion to the amount of added Ri-MuLV. These studies indicate a relationship between a change in virus tropism to NB by passage in certain hosts (e.g., Swiss/ICR mice) and the ability of Friend virus to induce erythroleukemia that spontaneously regresses. MuLV-RF isolated from the RFV complex induced lymphocytic leukemia in newborn mice which regressed and caused the regression of CFV-induced erythroleukemia. MuLV-RF is NB-tropic, contains no spleen focus-forming virus (SFFV) activity and helps SFFV form spleen foci in genetically restrictive mice. Pseudotype viruses were prepared, consisting of MuLV-RF, or other MuLV's, and SFFV derived from FV-B. The pseudotype viruses each acquired the tropism of the MuLV used in rescue. The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed. These studies demonstrate that the ability of RFV to induce erythroleukemia that spontaneously regresses is due to its helper MuLV component.
弗氏病毒复合体的RFV毒株可诱发一种能自发消退的红白血病。消退型弗氏病毒复合体(RFV)的嗜性由其辅助性莫洛尼鼠白血病病毒(MuLV)成分MuLV-RF决定,与传统病毒毒株CFV不同。RFV具有嗜NB特性,而CFV具有嗜N特性。非消退型CFV通过Fv-1不相容的瑞士/ICR小鼠传代后,其嗜性从N型转变为NB型,产生了一种能诱发可消退红白血病的病毒毒株。NB嗜性的CFV再通过Fv-1相容的小鼠传代后,仍保持NB嗜性和消退特性。通过添加Ri-MuLV改变RFV复合体中辅助性MuLV的数量或类型,会按添加的Ri-MuLV量抑制消退。这些研究表明,病毒在特定宿主(如瑞士/ICR小鼠)中传代后嗜性转变为NB型与弗氏病毒诱发能自发消退的红白血病的能力之间存在关联。从RFV复合体中分离出的MuLV-RF可诱发新生小鼠的淋巴细胞白血病,该白血病可消退,并能使CFV诱发的红白血病消退。MuLV-RF具有NB嗜性,不具有脾集落形成病毒(SFFV)活性,但能帮助SFFV在基因限制型小鼠中形成脾集落。制备了假型病毒,其由MuLV-RF或其他MuLV以及源自FV-B的SFFV组成。每种假型病毒都获得了用于拯救的MuLV的嗜性。用MuLV-RF或另一种NB嗜性的MuLV-F制备的假型病毒,但不是用N嗜性的MuLV-F拯救获得的病毒,可诱发能自发消退的红白血病。这些研究表明,RFV诱发能自发消退的红白血病的能力归因于其辅助性MuLV成分。