Abstract
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, non-infected 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.
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