Replication Cycle of Newcastle Disease Virus in Three Host Cells of Different Permissiveness

Abstract

SUMMARYVarious degrees of permissiveness for NDV have been described in different cell lines. In the present work three systems were investigated: bovine kidney (MDBK) cells, chick embryo (CE) cells and mouse L cells producing 50 to IOO p.f,U., 2 to IO p.f.u, and less than o.I p.f.u./cell, respectively. Analysis of the radioactive virus messenger RNAs (vmRNAs) accumulating in actinomycin D-treated cells throughout the infection cycle revealed that, except for the absence of one 18S vmRNA species in L cells, all vmRNA components were formed in the three cell types, although variations occurred in their total and relative amounts from one cell type to another. Kinetic studies of vmRNA synthesis confirmed the absence of one I8S vmRNA species in L cells and also showed that the labelling rate of this vmRNA component is higher in CE cells. Virus proteins synthesized in the infected cells were labelled with l~C-amino acids and analysed by polyacrylamide gel electrophoresis. All the major NDV polypeptides were formed as expected in both CE and MDBK cells but only traces were detected in L cells. In contrast in a cell-free translation system from wheat germ, all of the NDV major proteins were synthesized using RNA extracted from the three infected cell types. Moreover, the total radioactivity incorporated into NDV proteins was twice as great with CE cell RNA and five times as great with L cell RNA than with equivalent quantities of RNA from MDBK cells.

Relation of Interferon Production to the Limited Replication of Newcastle Disease Virus in L Cells

“…Some of these seemed to be carried out on the assumption that IFN might not be responsible for the limited virus growth. For example, the synthesis of viral RNA and proteins has been analysed in the presence of actinomycin D, an inhibitor of IFN production (Hecht & Summers, 1974, Gresland et al, 1979. Our results make it difficult to interpret these data unambiguously, until the possible influence of IFN on the virus replication is assessed in each case.…”