Roles of helper and defective retroviral genomes in murine erythroleukemia: Studies of spleen focus-forming virus in the absence of helper

R. K. Bestwick, W. D. Hankins, D. Kabat

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

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 (ψ2 cells). The transfected cells released virus (ψ2/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, ψ2/SFFV caused a rapid splenic erythroblastosis that regressed. Extensive erythroblastosis could be maintained by repeated injections of ψ2/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 ψ2/SFFV causes a wave of erythroblastosis. The properties of the proliferating erythroblasts are substantially determined by the R-SFFV viral component.

Original languageEnglish (US)
Pages (from-to)660-664
Number of pages5
JournalJournal of virology
Volume56
Issue number3
DOIs
StatePublished - 1985

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Fingerprint Dive into the research topics of 'Roles of helper and defective retroviral genomes in murine erythroleukemia: Studies of spleen focus-forming virus in the absence of helper'. Together they form a unique fingerprint.

  • Cite this