Effects of exogenous interferon on L cells persistently infected with Sendai virus.
A carrier culture of L cells persistently infected with Sendai virus (steady state) designated as L-Sendaits cells was established with a temperature-sensitive strain of the virus. When interferon was added to culture fluids from the start of the cultures at permissive (35 degrees C) or non-permissive temperature (38 degrees C), cell-associated infectivity was unaffected at 35 degrees C, while it was unexpectedly enhanced at 38 degrees C, although the cell-associated infectivity was titrated after further incubation at 32 degrees C for 2 days. The titer of cell-associated infectivity was increased by subculturing in the continuous presence of interferon at 38 degrees C. The effect of interferon on the paradoxical enhancement of cell-associated infectivity was shown to be dose dependent. When L-Sendaits cells were successively subcultured 6 times at 38 degrees C in the continuous presence or absence of interferon, more than 95 per cent of the cells contained a detectable amount of nucleocapsid (NP) antigen in the presence of interferon, whereas the antigen could be detected in only 30-40 per cent of the cells subcultured in the absence of interferon. Only when the cells subcultured at 38 degrees C in the presence of interferon were transferred to permissive temperature, could the distinct hemadsorbing and cell-associated hemagglutinating activities and the release of virus particles, as measured by hemagglutinating activity in the culture fluids, be detected. Cells subcultured in the presence of interferon accumulated more virus polypeptides than in the absence of interferon. Accumulation of virus specific RNA in the cells subcultured in the presence of interferon was about twice as much as that in the absence of interferon. Larger sized RNA (probably 50S) was the major species and two smaller RNAs could be detected in both the treated and untreated cells. When L-Sendaits cells were cultured at 38 degrees C in the presence of interferon, their multiplication was clearly inhibited. However, the cells which were subcultured twice at 38 degrees C in the continuous presence of interferon acquired resistance to the anti-cell proliferative action of interferon. Interestingly, the conversion of the sensitive state to resistant state of the cells was reversible.
D000818:Animals; D000956:Antigens, Viral / Q000032:analysis; D002213:Capsid / Q000276:immunology; D002455:Cell Division; D003593:Cytoplasm / Q000276:immunology; D006387:Hemagglutination, Viral; D007372:Interferons / Q000494:pharmacology*; D007739:L Cells; D051379:Mice; D010222:Parainfluenza Virus 1, Human / Q000254:growth & development* / Q000276:immunology / Q000378:metabolism; D012367:RNA, Viral / Q000096:biosynthesis; D013696:Temperature; D014764:Viral Proteins / Q000096:biosynthesis
D000956:Antigens, Viral; D012367:RNA, Viral; D014764:Viral Proteins; D007372:Interferons