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The synthesis of virus RNA and proteins in cells infected with two populations of defective virions [Pr(1)53 and Pr(2)53] which vary in the overall composition of their DNA, but which share some structural and biological characteristics, have been examined. The experiments were done under two sets of conditions: (1) at high multiplicity of infection. In this case, practically all the cells in the cultures were co-infected with defective and infectious virions; (2) at low multiplicity of infection. In this case, 75% of the cells in the cultures were infected with defective virions only and 25% were co-infected with defective and infectious virions. The relative abundance of RNA classes complementary to different regions of the virus genomes that were synthesized under various conditions of infection were determined by the Southern (1975) technique; the synthesis of virus proteins was determined by polyacrylamide gel electrophoresis (PAGE). In cells co-infected with standard and defective virions, RNA complementary to the regions that are reiterated in the defective genomes is present in larger amounts than in cells infected with standard virions alone, indicating that the genomes of the defective virions are transcribed. Furthermore, the transcriptional controls that operate normally in the infected cells also operate in cells co-infected with standard and defective virions. The over-abundant accumulation of transcripts of some regions of the virus genome in cells co-infected with defective virions is not necessarily accompanied by an overproduction of some virus proteins. No difference in the PAGE profiles of the proteins synthesized was detected in cells co-infected with PR(1)53 and standard virions. However, cells co-infected with standard and Pr(2)53 overproduced three polypeptides. Transcription of the virus genome is detectable in cells infected with Pr(2)53 alone but not in cells infected with Pr(2)53 alone. Virus protein synthesis is also detectable under these conditions in Pr(2)-, but not in Pr(1)-infected cells. Thus, despite the similarities in the biological characteristics of the two populations of defective virions described previously, similarities with respect to the expression of their genomes were not found.

Expression of the Genome of Defective Interfering Pseudorabies Virions in the Presence or Absence of Helper Functions Provided by Standard Virus