A Mouse Cell Line, which Is Unprotected by Interferon against Lytic Virus Infection, Lacks Ribonuclease F Activity

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Abstract
A mouse cell line, NIH 3T3, does not respond to some of the activities of interferon. Even after treatment with high concentrations of interferon, the replication of lytic viruses such as encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV) is not inhibited in these cells. Interferon treatment of these same cells results in the inhibition of Moloney murine leukemia virus (MMuLV) production. Enzymatic pathways which are induced by interferon in these cells were analyzed. After interferon treatment, the level of the (2''-5'')oligoadenylate [(2''-5'')An] synthetase activity and the phosphorylation of the 67,000 dalton protein (P1) are enhanced in NIH 3T3 cells to approximately the same level as interferon-sensitive mouse L-cells. NIH 3T3 and L-cells contain approximately the same levels of enzymes which inactivate (2''-5'')An. Both exogenously added (2''-5'')A3 or double-stranded RNA (dsRNA) failed to inhibit protein synthesis in NIH 3T3 extracts even though they were potent inhibitors of L-cell extract-directed protein synthesis. Direct measurements of the (2''-5'')An-dependent RNase F failed to detect such activity in NIH 3T3 cells. The presence of RNase F activity apparently is necessary for the interferon-induced antiviral activity against EMCV and VSV. The induction of protein kinase activity by interferon treatment of NIH 3T3 cells appears to have no direct effect on EMCV and VSV replication.