Effect of interferon on transient shut-off of cellular RNA and protein synthesis induced by Mengo virus infection.
Infection of mouse L929 cells with Mengo virus resulted in a rapid shut-off of cellular RNA synthesis followed within the first hours post infection by a gradual decrease in host protein synthesis. Pretreatment of the cells with high doses of interferon, blocking viral multiplication, did not affect the virus-induced shut-off of host macromolecular synthesis. In these interferon-treated cells the 2',5'A-activated nuclease may account for the degradation of viral RNA, soon after its replication. However, the inhibition of host protein synthesis could not be explained by this mechanism. Poly(A)-containing RNA, present in interferon-treated and infected cells, amounted to as much as 70% of that present in interferon-treated, noninfected cells. On the other hand, extracted cytoplasmic RNA was efficiently translated in a reticulocyte lysate, showing that extensive mRNA degradation was not involved in the inhibition of host protein synthesis. In the continued presence of interferon, the virus-induced shut-off was found to be transient. Late in infection, RNA synthesis was found to recover, followed by recovery of protein synthesis and survival of the cells.
D004769:Enterovirus Infections / Q000378:metabolism*; D007372:Interferons / Q000494:pharmacology*; D007700:Kinetics; D007739:L Cells / Q000378:metabolism; D046911:Macromolecular Substances; D008574:Mengovirus; D009693:Nucleic Acid Hybridization; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis* / Q000235:genetics; D013997:Time Factors
D046911:Macromolecular Substances; D012313:RNA; D007372:Interferons