Abstract
A comparison of the replication patterns in L cells and in chick embryo (CE) cell cultures was carried out with the Herts strain of Newcastle disease virus (NDVo) and with a mutant (NDVpi) isolated from persistently infected L cells. A significant amount of virus progeny, 11 plaque-forming units (PFU)/cell, was synthesized in L cells infected with NDVo, but the infectivity remained cell-associated and disappeared without being detectable in the medium. In contrast, in L cells infected with NDVpi, progeny virus (30 PFU/cell) was released efficiently upon maturation. It is suggested that the term “covert” rather than “abortive” be used to describe the infection of L cells with NDVo. In both L and CE cells, the latent period of NDVpi was 2 to 4 hr longer than for NDVo. The delay in synthesis of viral ribonucleic acid (RNA) in the case of NDVpi coincided with the delay in the inhibition of host RNA and protein synthesis. Although both NDVo and NDVpi produced more progeny and more severe cell damage in CE cells than in L cells, the shut-off of host functions was significantly less efficient in CE cells than in L cells. Paradoxically, no detectable interferon was produced in CE cells by either of the viruses, whereas in L cells most of the interferon appeared in the medium after more than 90% of host protein synthesis was inhibited. These results suggest that the absence of induction of interferon synthesis in CE cells infected with NDV is not related to the general shut-off of host cell synthetic mechanisms but rather to the failure of some more specific event to occur. In spite of the fact that NDVpi RNA synthesis commenced 2 to 4 hr later than that of NDVo, interferon was first detected in the medium 8 hr after infection with both viruses. This finding suggests that there is no relation between viral RNA synthesis and the induction of interferon synthesis.
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