Abstract

Two variant strains of a rabbit kidney cell line, RK-13, differ markedly in their interferon (IFN)-mediated antiviral mechanism. Both strains are permissive for the growth of vesicular stomatitis (VSV) and vaccinia viruses. Following treatment with 100 U/ml of rabbit IFN, both cell strains restrict VSV yield about a 1000-fold; vaccinia is not inhibited by IFN in either cell strain. However, vaccinia is able to rescue VSV from the inhibitory effects of IFN in one strain (RK-13), but not in the other strain of cells (RK-13-37). Investigation of the mechanism of this phenomenon reveals that VSV growth is blocked at different levels in the two cell strains. In the strain in which vaccinia can rescue VSV from the effects of IFN (RK-13), the major IFN-mediated restriction of VSV growth is at the level of protein synthesis; in the other strain in which vaccinia is unable to rescue VSV (RK-13-37), IFN restricts VSV at earlier steps, including penetration and primary transcription. The two cell strains provide useful models for studying the multifaceted nature of IFN-mediated antiviral effects.

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