Literature DB >> 28371814

The duck enteritis virus early protein, UL13, found in both nucleus and cytoplasm, influences viral replication in cell culture.

X Hu1,2,3, M Wang1,2,3, S Chen1,2,3, R Jia1,2,3, D Zhu2,3, M Liu1,2,3, Q Yang1,2,3, K Sun1,2,3, X Chen2,3, A Cheng1,2,3.   

Abstract

The UL13 protein of the duck enteritis virus (DEV), predicted to encode a Ser/Thr protein kinase, belongs to the family of conserved herpesvirus protein kinases (CHPK), which plays an important role in herpesvirus proliferation. In this study, truncated UL13 was expressed as a fusion protein of approximately 44 kDa using a prokaryotic expression system, and this protein was used to generate a specific anti-UL13 antibody. This antibody detected UL13 starting at 4 h post infection in duck embryonic fibroblast cells and identified UL13 to be present in both the cytoplasm and the nucleus. UL13 RNA was found to be transcribed starting at 2 h post infection, and the synthesis of the UL13 mRNA was found to be sensitive to the protein synthesis inhibitor cycloheximide (CHX) and tolerant of the DNA polymerase inhibitor ganciclovir (GCV). Its nuclear location and status as an early gene suggested that DEV UL13 might play important roles in DEV replication, which was confirmed by comparing the proliferation of a UL13-knockout mutant virus, a revertant virus, and the parent virus in cell culture. The specific mechanisms of UL13 in viral replication need to be further studied.
© 2017 Poultry Science Association Inc.

Entities:  

Keywords:  UL13; duck enteritis virus; early gene; intracellular location; mutant virus

Mesh:

Substances:

Year:  2017        PMID: 28371814     DOI: 10.3382/ps/pex043

Source DB:  PubMed          Journal:  Poult Sci        ISSN: 0032-5791            Impact factor:   3.352


  8 in total

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Journal:  Front Cell Infect Microbiol       Date:  2020-01-17       Impact factor: 5.293

8.  Duck enteritis virus pUL47, as a late structural protein localized in the nucleus, mainly depends on residues 40 to 50 and 768 to 777 and inhibits IFN-β signalling by interacting with STAT1.

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  8 in total

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