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Duck plague virus Us3 regulates the expression of pUL48.

ABSTRACT: Duck plague (DP) is one of the contagious diseases caused by Duck plague virus (DPV), which is a serious threat to the development of duck farming. Us3 is a PKA-like protein kinase in alphaherpesvirus, which can regulate the biological functions of many viral proteins, but whether Us3 regulates pUL48 protein has not been reported. In this paper, Western Blot, qRT-PCR, dual luciferase reporter system and Co-IP were used to investigate the relationship between pUL48 and Us3. The results showed that: 1) pUL48 interacted with Us3 at 138-256aa through its DBD region. 2) Us3 enhanced the protein expression of pUL48 in a dose-dependent manner. 3) Us3 promoted the mRNA level of pUL48 by activating its promoter activity. 4) Us3 inhibited the transcriptional activation function of pUL48. The results can provide scientific data for perfecting and supplementing the function of alpha herpesvirus Us3 and pUL48.

SUBMITTER: Zhou T

PROVIDER: S-EPMC10879799 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature

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Duck plague virus Us3 regulates the expression of pUL48.

Zhou Tong T Ruan Peilin P Wang Mingshu M Cheng Anchun A Zhang Wei W Tian Bin B Yang Qiao Q Ou Xumin X Sun Di D He Yu Y Wu Zhen Z Zhang Shaqiu S Huang Juan J Wu Ying Y Zhao Xin-Xin XX Yu Yanling Y Zhang Ling L Zhu Dekang D Chen Shun S Liu Mafeng M Jia Renyong R

Poultry science 20240126 4

Duck plague (DP) is one of the contagious diseases caused by Duck plague virus (DPV), which is a serious threat to the development of duck farming. Us3 is a PKA-like protein kinase in alphaherpesvirus, which can regulate the biological functions of many viral proteins, but whether Us3 regulates pUL48 protein has not been reported. In this paper, Western Blot, qRT-PCR, dual luciferase reporter system and Co-IP were used to investigate the relationship between pUL48 and Us3. The results showed tha ...[more]

PMID: 38364609

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Project description:Duck plague virus (DPV) is a member of the alphaherpesvirus subfamily, and its genome encodes a conserved envelope protein, protein UL10 (pUL10). pUL10 plays complex roles in viral fusion, assembly, cell-to-cell spread, and immune evasion, which are closely related to its protein characteristics and partners. Few studies have been conducted on DPV pUL10. In this study, we identified the characteristics of pUL10, such as the type of glycosylation modification and subcellular localization. The characteristic differences in pUL10 in transfection and infection suggest that there are other viral proteins that participate in pUL10 modification and localization. Therefore, pUL49.5, the interaction partner of pUL10, was explored. We found that pUL10 interacts with pUL49.5 during transfection and infection. Their interaction entailed multiple interaction sites, including noncovalent forces in the pUL49.5 N-terminal domains and C-terminal domains and a covalent disulfide bond between two conserved cysteines. pUL49.5 promoted pUL10 expression and mature N-linked glycosylation modification. Moreover, deletion of UL49.5 in DPV caused the molecular mass of pUL10 to decrease by approximately3 to 10 kDa, which suggested that pUL49.5 was the main factor affecting the N-linked glycosylation of DPV pUL10 during infection. This study provides a basis for future exploration of the effect of pUL10 glycosylation on virus proliferation. IMPORTANCE Duck plague is a disease with high morbidity and mortality rates, and it causes great losses for the duck breeding industry. Duck plague virus (DPV) is the causative agent of duck plague, and DPV UL10 protein (pUL10) is a homolog of glycoprotein M (gM), which is conserved in herpesviruses. pUL10 plays complex roles in viral fusion, assembly, cell-to-cell spread, and immune evasion, which are closely related to its protein characteristics and partners. In this study, we systematically explored whether pUL49.5 (a partner of pUL10) plays roles in the localization, modification, and expression of pUL10.

Project description:BackgroundDuck plague virus (DPV), belonging to herpesviruses, is a linear double-stranded DNA virus. There are many reports about the outbreak of the duck plague in a variety of countries, which caused huge economic losses. Recently, increasing reports revealed that multiple long non-coding RNAs (lncRNAs) can possess great potential in the regulation of host antiviral immune response. Furthermore, it remains to be determined which specific molecular mechanisms are responsible for the DPV-host interaction in host immunity. Here, lncRNAs and mRNAs in DPV infected duck embryonic fibroblast (DEF) cells were identified by high-throughput RNA-sequencing (RNA-seq). And we predicted target genes of differentially expressed genes (DEGs) and formed a complex regulatory network depending on in-silico analysis and prediction.ResultRNA-seq analysis results showed that 2921 lncRNAs were found at 30 h post-infection (hpi). In our study, 218 DE lncRNAs and 2840 DE mRNAs were obtained in DEF after DPV infection. Among these DEGs and target genes, some have been authenticated as immune-related molecules, such as a Macrophage mannose receptor (MR), Anas platyrhynchos toll-like receptor 2 (TLR2), leukocyte differentiation antigen, interleukin family, and their related regulatory factors. Furthermore, according to the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis, we found that the target genes may have important effects on biological development, biosynthesis, signal transduction, cell biological regulation, and cell process. Also, we obtained, the potential targeting relationship existing in DEF cells between host lncRNAs and DPV-encoded miRNAs by software.ConclusionsThis study revealed not only expression changes, but also the possible biological regulatory relationship of lncRNAs and mRNAs in DPV infected DEF cells. Together, these data and analyses provide additional insight into the role of lncRNAs and mRNAs in the host's immune response to DPV infection.

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Duck plague virus Us3 regulates the expression of pUL48.

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Duck plague virus Us3 regulates the expression of pUL48.

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