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We have studied protein synthesis in cultured cells infected with the six noncytopathic (nc ) mutants of the Australia-Victoria strain (AV-WT) of Newcastle disease virus and their plaque-forming revertants. Virus-specific polypeptides accumulated at 30 to 63% of wild-type levels innc mutant-infected cells and between 66 and 175% of wild-type levels in revertant-infected cells. An exception was the L polypeptide, which accumulated innc mutant-infected cells at only 5 to 20% of the levels found in wild-type infection. The reduced accumulation of the L polypeptide did not appear to be due to increased degradation of that polypeptide. A new polypeptide (X) accumulated instead of polypeptide P in cells infected with mutantsnc 4 ornc 16 and in virions released from them. Peptide mapping identified X as an altered form of P. A revertant of mutantnc 4 (nc 4S1), which forms larger hemadsorbing spots, but still does not form plaques, accumulated P instead of the X polypeptide. Thus, a lesion in P can affect virus spread without affecting cytopathogenicity. Virions of mutantnc 7 and two naturally occurring avirulent strains of Newcastle disease virus (NJ LaSota and B1-Hitchner) contained polypeptides (F7 and FA , respectively) related to, but migrating more rapidly than, F0 in sodium dodecyl sulfate-polyacrylamide gels. As previously reported for avirulent strains, a brief treatment ofnc 7 virions with trypsin converted F7 to F and increased infectivity. Similarly, culturingnc 7-infected cells in the presence of trypsin facilitated fusion from within and viral spread from cell to cell. A plaque-forming revertant ofnc 7 still accumulated F7 in virions, indicating that the lesions responsible for the F7 and noncytopathic phenotypes are genetically separable. The virulent parental strain, AV-WT, exhibited a mean embryo death time of 42 h. Both the larger-spot-forming revertant ofnc 4 (nc 4S1) and the small-plaque-forming revertant ofnc 7 exhibited a decrease in mean embryo death time (increase in virulence) from 74 to 63 h. A second-step, plaque-forming revertant derived fromnc 4S1 (nc 4S1R1) exhibited a further decrease in mean embryo death time from 63 to 44 h. The results suggest that the FA -F7 and X lesions affect the ability of virus to spread from cell to cell. In addition, these lesions appear to be genetically separable from those responsible for the noncytopathic phenotype. However, both types of lesions cause an extension of mean embryo death time and, thus, may be relevant to virulence in vivo.

Relationships Among Virus Spread, Cytopathogenicity, and Virulence as Revealed by the Noncytopathic Mutants of Newcastle Disease Virus