Identification and characterization of duck plague virus glycoprotein C gene and gene product

Xu, Chao; Cheng, Anchun; Wang, Mingshu; Zhu, Dekang; Luo, Qihui; Jia, Renyong; Bi, Feng-jun; Chen, Zhengli; Zhou, Yi; Yang, Zexiao; Chen, Xiaoyue

doi:10.1186/1743-422x-7-349

Cited by 28 publications

(23 citation statements)

References 46 publications

(25 reference statements)

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“…The virulent strain of DEV can be adapted by several passages in duck embryo and chicken embryo fibroblast (CEF) cell culture (John et al 1990;Mondal et al 2010;Doley et al 2013). Naturally apathogenic or attenuated DEV strains are being used as live vaccines that can offer sufficient protection for commercial ducks Jansen 1968;Spieker 1977;Lin et al 1984;Liu et al 2007;Lian et al 2010). Mostly the virus is propagated, adapted and passaged in homologous host/cell culture of avian (duck/chicken) origin for large scale vaccine production but recently DEV has been grown successfully over Vero cell lines (green monkey origin) as evident from cytopathic effects and identification of DNA and viral antigens by polymerase chain reaction (PCR) and indirect immunofluorescence (IF) techniques .…”

Section: Introductionmentioning

confidence: 99%

Duck virus enteritis (duck plague) – a comprehensive update

Dhama

Kumar

Saminathan

et al. 2017

Veterinary Quarterly

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Duck virus enteritis (DVE), also called duck plague, is one of the major contagious and fatal diseases of ducks, geese and swan. It is caused by duck enteritis virus (DEV)/Anatid herpesvirus-1 of the genus Mardivirus, family Herpesviridae, and subfamily Alpha-herpesvirinae. Of note, DVE has worldwide distribution, wherein migratory waterfowl plays a crucial role in its transmission within and between continents. Furthermore, horizontal and/ or vertical transmission plays a significant role in disease spread through oral-fecal discharges. Either of sexes from varying age groups of ducks is vulnerable to DVE. The disease is characterized by sudden death, vascular damage and subsequent internal hemorrhage, lesions in lymphoid organs, digestive mucosal eruptions, severe diarrhea and degenerative lesions in parenchymatous organs. Huge economic losses are connected with acute nature of the disease, increased morbidity and mortality (5%-100%), condemnations of carcasses, decreased egg production and hatchability. Although clinical manifestations and histopathology can provide preliminary diagnosis, the confirmatory diagnosis involves virus isolation and detection using serological and molecular tests. For prophylaxis, both live-attenuated and killed vaccines are being used in broiler and breeder ducks above 2 weeks of age. Since DEV is capable of becoming latent as well as shed intermittently, recombinant subunit and DNA vaccines either alone or in combination (polyvalent) are being targeted for its benign prevention. This review describes DEV, epidemiology, transmission, the disease (DVE), pathogenesis, and advances in diagnosis, vaccination and antiviral agents/therapies along with appropriate prevention and control strategies.

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Section: Introductionmentioning

confidence: 99%

Duck virus enteritis (duck plague) – a comprehensive update

Dhama

Kumar

Saminathan

et al. 2017

Veterinary Quarterly

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“…To express gB, gC, or gE, Escherichia coli strains were transformed with pET28a-gB, pET32a-gC, or pET32a-gE vectors constructed previously (Chang et al 2010;Lian et al 2010). Briefly, pET28a-gB transformed E. coli DE3 cells incubated in 1.5 L of LB/Kana broth were induced with 0.2 mmol L -1 IPTG for 2.5 h at 37°C.…”

Section: The Interaction Of Glycoprotein C With Cell Surface Hsmentioning

confidence: 99%

Role of duck plague virus glycoprotein C in viral adsorption: Absence of specific interactions with cell surface heparan sulfate

Jing

Sun

et al. 2017

Journal of Integrative Agriculture

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Many mammalian herpes viruses utilize heparan sulfate (HS) moieties present on cell surface proteoglycans as receptors for cell entry, and this process also requires viral glycoprotein C (gC) homologues. However, our understanding of the role of gC in facilitating attachment of other alpha-herpes viruses such as the duck plague virus (DPV) remains preliminary. To study the role of gC during DPV infection, we used a gC-deleted mutant virus (DPV-ΔgC-EGFP). Examination of the viral copy number by real-time PCR, as well as time course studies of viral adsorption and proliferation revealed that gC was involved in the viral binding to the cell surface. The affinity of viral glycoproteins (gB-DPV, gC-DPV, and gE-DPV) to HS was assessed using a prokaryotic expression system and HiTrap TM Heparin HP column chromatography. In addition, to confirm that gC played a role in the interaction between DPV and HS, viruses were treated with the HS analogue heparin and host cells were treated with its inhibitors heparinase prior to exposure to DPV-ΔgC-EGFP or wild-type strain Chinese virulent duck plague virus (DPV-CHv). The effects of heparin and heparinase on virus infectivity demonstrated that function of gC on viral adsorption is independent of interactions between gC and heparin sulfate on cell surface. All in all, this study demonstrated that the gC of DPV can mediate viral adsorption in an HS-independent manner, which distinguish it from the gC of some other alpha-herpes viruses. Future studies will be required to identify the receptors involved in gC protein binding to cells. This work provides us a foundation for further studies of examining the roles of gC in the adsorption during duck plague virus infection.

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“…The primers used for qRT-PCR were ΔUS2 F (5'-AGACGGTTCCGAAAGTACAG-3') and US2 R (5'-TCGGCAGCACCAATAATCC-3'), β-actin F (5'-CCGGGCATCGCTGACA-3') and β-actin R (5'-GGATTCATCATACTCCTGCTTGCT-3'). The in vitro transcriptional level of the DEV US2 gene was detected by a previously described qRT-PCR process (Lian et al, 2010). The optimized 20 μL real-time PCR mixture comprised 1 μL (10 pM) of each primer, 1 μL DNA template, 10 μL SYBR Green I Mix, and 7 μL autoclaved double-filtered nanopure water.…”

Section: Transcriptional Levels Of the Us2 Genementioning

confidence: 99%

Identification and characterization of the duck enteritis virus (DEV) US2 gene

Gao¹,

Cheng²,

Wang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The US2 protein has been reported to contribute to duck enteritis virus (DEV) infection; however, its kinetics and localization during infection, and whether it is a component of virion, have not been previously reported. To elucidate the function of DEV US2, US2 was amplified by polymerase chain reaction (PCR) and inserted into pET-32a(+); this was expressed, the recombinant US2 protein was purified, and a polyclonal antibody generated. In addition, the kinetics and localization of the US2 gene and protein were determined by quantitative real-time fluorescent PCR, ganciclovir (GCV), and cycloheximide (CHX) treatment, westernblot, and indirect immunofluorescence assay. The packaging of US2 into DEV virions was revealed by a protease protection assay. US2 was found to be transcribed 24 h post-infection (pi) and peaked at 72 h pi; the US2 protein was detected 48 h pi, except in the presence of GCV or CHX. US2 was packed into virions and also localized to the plasma membrane and 13779-13790 (2015) cytoplasm in infected cells. The results showed that the DEV US2 is a late gene, and that its encoding protein could be a tegument component localized mainly in the cytoplasm. This study provides useful data for the further analysis of DEV US2, including an explanation for the genetic conservation among alphaherpesviruses.

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Identification and characterization of duck plague virus glycoprotein C gene and gene product

Cited by 28 publications

References 46 publications

Duck virus enteritis (duck plague) – a comprehensive update

Duck virus enteritis (duck plague) – a comprehensive update

Role of duck plague virus glycoprotein C in viral adsorption: Absence of specific interactions with cell surface heparan sulfate

Identification and characterization of the duck enteritis virus (DEV) US2 gene

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