Key result
Deletion of the duck enteritis virus UL54 gene significantly impaired viral growth, reduced plaque size, and altered viral gene transcription and translation.
The DEV UL54 gene is essential for viral replication and regulates viral gene expression during transcription, mRNA export, and translation.
UL54 deletion confirms essential role in DEV replication; leaves open targeted antiviral or vaccine strategies pending in vivo studies.
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.
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Liu et al. (2017) studied Duck enteritis virus (DEV) infection. UL54 gene deletion (DEV-ΔUL54) vs. Wild-type DEV (DEV-LoxP) and revertant virus was evaluated on Viral growth kinetics, plaque size, and viral DNA copy number. Deletion of the duck enteritis virus UL54 gene significantly impaired viral growth, reduced plaque size, and altered viral gene transcription and translation.
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