The triggering mechanism for interferon synthesis in mouse peritoneal macrophages and chick embryo (CE) cells by Newcastle disease virus (NDV) exposed to hydroxylamine or homologous antiserum was investigated in relation to the intracellular fate of these agents.

Inactivation of NDV at 22 °C by 1 -hydroxylamine proceeded with first-order kinetics, whereas the interferon-inducing capacity of hydroxylamine-treated virus in macrophages was unimpaired. In contrast to infective NDV, hydroxylamine-inactivated virus produced interferon in CE cells, and such a virus still had partial RNA-dependent RNA polymerase activity. Hydroxylamine-inactivated NDV was adsorbed to and uncoated in both normal and chloroquine diphosphate treated cells, but no viral double-stranded RNA was detected. Hydroxylamine treatment of virion-extracted RNA and neutralization of intact virions by antibody abolished the capacity of the virus to induce interferon. Infective as well as neutralized NDV interacted with macrophages to the same degree, but association between NDV and CE cells was prevented by antibody-coating. In macrophages, the RNA of neutralized NDV became more sensitive to RNase than RNA of infective NDV, but this process was inhibited in chloroquine diphosphate-treated cells. These results suggest that interferon induction by NDV involves components of the virion which are present up to the regular uncoating process.


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