Accumulation and breakdown of RNA-deficient intracellular virus particles in interferon-treated NIH 3T3 cells chronically producing Moloney murine leukemia virus.
Interferon treatment of NIH 3T3 cells chronically infected with Moloney murine leukemia virus inhibited about 95% of virus release. This inhibition was accompanied by a three- to twofold accumulation of intracellular virions. However, this accumulation could be demonstrated only be exogenous reverse transcriptase reaction assay or radioactive labeling of the assembled viral proteins. It could not be shown by the endogenous reverse transcriptase reaction assay, which depended on endogenous viral RNA, or by labeling the encapsidated viral RNA. It was therefore evident that most of the intracellular virions accumulated in interferon-treated cells were RNA deficient. Hybridization analysis revealed that these virions were deficient of genomic viral RNA, whereas size analysis by gel electrophoresis suggested that the deficiency of 4S RNA normally packaged in Moloney murine leukemia virus was even stronger. Our data also suggested that this RNA deficiency was not due to degradation of the encapsidated RNA, but more likely to a defect in virus assembly. RNA-lacking intracellular virions were unstable; they were found to collapse before being released.
D000818:Animals; D002478:Cells, Cultured; D007372:Interferons / Q000494:pharmacology*; D051379:Mice; D008979:Moloney murine leukemia virus / Q000187:drug effects* / Q000201:enzymology / Q000254:growth & development; D009024:Morphogenesis; D012367:RNA, Viral / Q000378:metabolism*; D012194:RNA-Directed DNA Polymerase / Q000032:analysis; D014771:Virion / Q000187:drug effects; D014779:Virus Replication / Q000187:drug effects*
D012367:RNA, Viral; D007372:Interferons; D012194:RNA-Directed DNA Polymerase