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Background  Pseudorabies virus (PRV), an alpha-herpesvirus of swine, is a widely used model organism in investigations of the molecular pathomechanisms of the herpesviruses. This work is the continuation of our earlier studies, in which we investigated the effect of the abrogation of gene function on the viral transcriptome by knocking out PRV genes playing roles in the coordination of global gene expression of the virus. In this study, we deleted the  us1  gene encoding the ICP22, an important viral regulatory protein, and analyzed the changes in the expression of other PRV genes.    Results  A multi-timepoint real-time RT-PCR technique was applied to evaluate the impact of deletion of the PRV  us1  gene on the overall transcription kinetics of viral genes. The mutation proved to exert a differential effect on the distinct kinetic classes of PRV genes at the various stages of lytic infection. In the  us1  gene-deleted virus, all the kinetic classes of the genes were significantly down-regulated in the first hour of infection. After 2 to 6 h of infection, the late genes were severely suppressed, whereas the early genes were unaffected. In the late stage of infection, the early genes were selectively up-regulated. In the mutant virus, the transcription of the  ie180  gene, the major coordinator of PRV gene expression, correlated closely with the transcription of other viral genes, a situation which was not found in the wild-type ( wt ) virus. A 4-h delay was observed in the commencement of DNA replication in the mutant virus as compared with the  wt  virus. The rate of transcription from a gene normalized to the relative copy number of the viral genome was observed to decline drastically following the initiation of DNA replication in both the  wt  and mutant backgrounds. Finally, the switch between the expressions of the early and late genes was demonstrated not to be controlled by DNA replication, as is widely believed, since the switch preceded the DNA replication.    Conclusions  Our results show a strong dependence of PRV gene expression on the presence of functional  us1  gene. ICP22 is shown to exert a differential effect on the distinct kinetic classes of PRV genes and to disrupt the close correlation between the transcription kinetics of  ie180  and other PRV transcripts. Furthermore, DNA replication exerts a severe constraint on the viral transcription.

The ICP22 protein selectively modifies the transcription of different kinetic classes of pseudorabies virus genes