Roles of helper and defective retroviral genomes in murine erythroleukemia: studies of spleen focus-forming virus in the absence of helper.
Retroviruses that cause acute oncogenesis are generally complexes of a replication-competent helper virus and a replication-defective component. However, the pure defective components have not been previously available. We prepared the defective spleen focus-forming virus component of Rauscher erythroleukemia virus (R-SFFV) by transfecting a colinear R-SFFV DNA clone into a retroviral packaging cell line (psi 2 cells). The transfected cells released virus (psi 2/SFFV) that was free of helper virus and that induced erythropoietin-dependent erythroid burst formation in bone marrow cultures. When injected into normal adult NIH/Swiss mice in moderate doses, psi 2/SFFV caused a rapid splenic erythroblastosis that regressed. Extensive erythroblastosis could be maintained by repeated injections of psi 2/SFFV into anemic mice or by the addition of a helper virus. We conclude that R-SFFV alone causes proliferation but not immortalization of a population of erythroblasts that is normally replenished from a precursor stem cell pool. Because these precursor cells are inefficiently infected, a single moderate inoculum of psi 2/SFFV causes a wave of erythroblastosis. The properties of the proliferating erythroblasts are substantially determined by the R-SFFV viral component.
D000818:Animals; D002460:Cell Line; D004920:Erythropoiesis / Q000187:drug effects; D004921:Erythropoietin / Q000494:pharmacology; D006378:Helper Viruses / Q000502:physiology; D009052:Leukemia Virus, Murine / Q000472:pathogenicity*; D004915:Leukemia, Erythroblastic, Acute / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D011925:Rauscher Virus / Q000472:pathogenicity*; D013154:Spleen / Q000473:pathology; D013155:Spleen Focus-Forming Viruses / Q000472:pathogenicity*; D014759:Viral Envelope Proteins / Q000096:biosynthesis; D014779:Virus Replication
D014759:Viral Envelope Proteins; D004921:Erythropoietin