Anand R, Steeves R A, Lilly F
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Microbios. 1989;58(235):71-82.
The interaction between defective spleen focus-forming virus (SFFV) and helper virus(es) in Friend virus (FV) complex has been assumed to be one-way, with the helper virus complementing SFFV by supplying necessary virion components. To test this assumption the expression of both SFFV and helper virus in partially congenic mice which differ at the Fv-2 locus, a gene that specifically controls susceptibility to SFFV, was analysed. When the mice were infected with LLV (a strain of Friend SFFV-free helper virus), there was no detectable effect of Fv-2 genotype on LLV expression as tested by virus infectivity in the XC plaque assay or by quantitative viral antigen analysis in an immunoprecipitation assay. However, after infection with FV complex there was an amplification of LLV (as well as SFFV) synthesis in Fv-2s as compared with Fv-2r hosts. To determine whether the increased LLV synthesis in Fv-2s mice was due to an increased population of susceptible target cells as a result of SFFV infection and/or transformation, the ratios of LLV-infected cells in the spleens of LLV- and FV-infected Fv-2s hosts in an infectious centre assay, were compared. Since the percentage of LLV-infected cells was equivalent in both instances, the higher rate of LLV synthesis after infection with FV complex was presumably due to intrinsic properties of SFFV-infected erythroid cells.
在弗氏病毒（FV）复合体中，缺陷型脾集落形成病毒（SFFV）与辅助病毒之间的相互作用一直被认为是单向的，即辅助病毒通过提供必要的病毒体成分来补充SFFV。为了验证这一假设，我们分析了在Fv - 2位点存在差异的部分同源小鼠中SFFV和辅助病毒的表达情况，Fv - 2基因专门控制对SFFV的易感性。当用LLV（一种无弗氏SFFV的辅助病毒株）感染小鼠时，通过XC空斑试验中的病毒感染性或免疫沉淀试验中的定量病毒抗原分析检测发现，Fv - 2基因型对LLV表达没有可检测到的影响。然而，在用FV复合体感染后，与Fv - 2r宿主相比，Fv - 2s宿主中LLV（以及SFFV）的合成出现了扩增。为了确定Fv - 2s小鼠中LLV合成增加是否是由于SFFV感染和/或转化导致易感靶细胞群体增加，我们在感染中心试验中比较了LLV感染的Fv - 2s宿主和FV感染的Fv - 2s宿主脾脏中LLV感染细胞的比例。由于在这两种情况下LLV感染细胞的百分比相当，因此在用FV复合体感染后LLV合成率较高可能是由于SFFV感染的红系细胞的内在特性所致。
