Replication of Radiation-Induced Murine Leukemia Virus in Normal and Transformed Mouse Cells
AUTOR(ES)
Nomura, Shigeko
RESUMO
Autonomous radiation-induced leukemia virus (RadLV) replication could be detected in mouse 3T3 cells by the development of interference with murine sarcoma virus (MSV), the appearance of covert helper activity for defective MSV, and by the induction of cytopathic effect type foci in MSV-transformed, leukemia virus-negative (S+L−) cells. A chronic infection of either 3T3 or S+L− cells with RadLV could be established. Both RadLV infectivity and helper activity were demonstrated in the same peak at a buoyant density of 1.16 g/cm3. Additionally a soluble inhibitor of MSV focus formation was found which could be separated from infectious RadLV. Examination of cell clones derived from chronically infected 3T3 cells showed that essentially every cell was infected and produced both infectious RadLV and low levels of inhibitor. Quantitative comparisons of autonomously replicating RadLV in normal 3T3 and S+L− cells suggested that RadLV may consist of several populations of virus of varying replicative potential. Apparently 99% of RadLV can be assayed only as helper units in normal cells or as replicative units in S+L− cells. To explain the atypical results, a model for RadLV deficiency is proposed.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=356324Documentos Relacionados
- Specificity of cell surface virus receptors on radiation leukemia virus and radiation-induced thymic lymphomas.
- Rescue of the defective murine sarcoma virus genome by radiation-induced leukemia virus from C57BL mice.
- Radiation-induced mutations at mouse hemoglobin loci.
- The ionizing radiation-induced replication protein A phosphorylation response differs between ataxia telangiectasia and normal human cells.
- Radiation-Induced Presumed Somatic Mutations in the House Mouse