Abstract

Duck enteritis virus (DEV) UL54 is a homologue of human herpes simplex virus-1 (HSV-1) ICP27, which plays essential regulatory roles during infection. Our previous studies indicated that DEV UL54 is an immediate-early protein that can shuttle between the nucleus and the cytoplasm. In the present study, we found that UL54-deleted DEV (DEV-ΔUL54) exhibits growth kinetics, a plaque size and a viral DNA copy number that are significantly different from those of its parent wild-type virus (DEV-LoxP) and the revertant (DEV-ΔUL54 (Revertant)). Relative viral mRNA levels, reflecting gene expression, the transcription phase and the translation stage, are also significantly different between DEV-ΔUL54-infected cells and DEV-LoxP/DEV-ΔUL54 (Revertant)-infected cells. However, the localization pattern of UL30 mRNA is obviously changed in DEV-ΔUL54-infected cells. These findings suggest that DEV UL54 is important for virus growth and may regulate viral gene expression during transcription, mRNA export and translation.

Highlights

  • Duck enteritis virus (DEV), known as duck plague virus (DPV), is an extensively studied alpha-herpesvirus

  • Examination of the growth kinetics, plaque size and viral DNA copy number of three DEV-derived viruses generated by employing the Red recombination system showed a smaller plaque area, a lower viral titre and a lower viral DNA copy number for DEV-ΔUL54, which could be recovered

  • The results showed that DEV UL54 could regulate viral gene expression either positively or negatively

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Summary

Introduction

Duck enteritis virus (DEV), known as duck plague virus (DPV), is an extensively studied alpha-herpesvirus. As a conserved protein[5], herpes simplex virus-1 (HSV-1) ICP27, a homologue of UL54, is required for viral replication[6] This protein possesses a shuttling property with nuclear and cytoplasmic activities; as a result, ICP27 is multi- functional, playing roles in both the positive and the negative regulation of expression of different target genes[7,8,9,10]. ICP27 has been identified to promote genomic DNA replication, which occurs in the nucleus[31] These findings show that HSV-1 ICP27 is important for modulating the biogenesis of DNA and mRNA, which is necessary for virus growth. The results showed that DEV UL54 could inhibit or enhance viral gene expression, transcription and translation and promote the export of UL30 mRNA.

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