Author
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MORIUCHI, HIROYUKI - NATIONAL INST. HEALTH |
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MORIUCHI, MASAKO - NATIONAL INST. HEALTH |
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DEAN, HANSI - MALLINCKRODT VET., INC. |
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Cheung, Andrew |
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COHEN, JEFFREY - NATIONAL INST. HEALTH |
Submitted to: Virology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 6/1/1995 Publication Date: N/A Citation: N/A Interpretive Summary: Pseudorabies virus (PRV) is a pathogen of swine. PRV is a herpesvirus which is genetically similar to some human herpesviruses whose genome sequences have been determined. However, the complete sequence of the PRV genome has not been determined, and therefore, the identities and functions of most PRV genes are unknown. The present study provides information on the function of the early protein 0 gene, which is important for virus replication. This work is important because it advances our knowledge of the genetic content of PRV and provides the basis for researchers to design intervention measures (e.g. vaccines) that will disrupt the PRV productive and latent infection processes. Technical Abstract: Pseudorabies virus (PRV) early protein 0 (EP0) is the homolog of varicella-zoster (VZV) open reading frame 61 (ORF61) protein and herpes simplex virus type 1 (HSV-1) ICP0. A PRV EP0 deletion mutant grows poorly in cell culture, suggesting that EP0 plays a critical role in the viral replicative cycle. In this study, we have shown that the growth defect of an EP0 deletion mutant was complemented in Vero cells expressing VZV ORF61 protein or HSV-1 ICP0. In transient expression assays PRV EP0, like VZV ORF61 protein and HSV-1 ICP0, transactivates a variety of promoters from PRV, VZV, HSV, and unrelated viruses. These data indicate that PRV EP0 is functionally homologous to VZV ORF61 protein and HSV-1 ICP0. |