Growth of Serotypes I and II and Variant Strains of Infectious Bursal Disease Virus in Vero Cells

1988 ◽  
Vol 32 (2) ◽  
pp. 298 ◽  
Author(s):  
F. S. B. Kibenge ◽  
A. S. Dhillon ◽  
R. G. Russell
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Vero Cells ◽  
Infectious Bursal Disease ◽  
Bursal Disease

scholarly journals Immunogenicity and Efficacy Evaluation of Vero Cell-Adapted Infectious Bursal Disease Virus LC-75 Vaccine Strain in Ethiopia 

2021 ◽  
Author(s):  
Wakjira Kebebe ◽  
Molalegne Bitew ◽  
Fufa Dawo ◽  
Bedaso Mammo ◽  
Hawa Mohammed ◽  
...  
Keyword(s):  
Vero Cell ◽  
Disease Virus ◽  
Vaccine Strain ◽  
Infectious Bursal Disease Virus ◽  
Chicken Embryo Fibroblast ◽  
Vero Cells ◽  
Infectious Bursal Disease ◽  
Efficacy Evaluation ◽  
Viral Pathogen ◽  
Bursal Disease

Abstract Background: Infectious bursal disease virus (IBDV) is an avian viral pathogen that causes infectious bursal disease (IBD) of chickens. The disease is endemic in Ethiopia since 2002 and vaccination is the major means of disease prevention and control. IBD vaccine is produced in Ethiopia using primary chicken embryo fibroblast (CEF) cell; which is time-consuming, laborious, and uneconomical. The present study was carried out to develop cell-based IBDV LC-75 vaccine using Vero cells, and to evaluate the immunogenicity and protection level.Results: Identity of the vaccine seed was confirmed using gene-specific primers using reverse transcription polymerase chain reaction. Confluent monolayer of Vero cells was infected with vaccine virus and serial passage continued till passage ten. Characteristic virus induced cytopathic effect was observed starting from passage 2 on the third day post-infection. The infectious titer of adapted virus showed a linear increment along the passage level. Virus induced specific antibody was determined using indirect ELISA after vaccination of 14 days old chicks through ocular route. Accordingly, the antibody titer measured from Vero cells vaccinated chicks revealed similar level with the currently available CEF cell-based vaccine. Chicks vaccinated with Vero cell adapted virus showed complete protection against very virulent IBDV, while unvaccinated group had 60% morbidity and 25% mortality.Conclusions: The IBDV vaccine strain well adapted on Vero cells and found to be immunogenic induces antibodies development and successfully protects chicks against challenging with the circulating field IBDV isolate. Hence, it is recommended to produce IBD vaccine using Vero cell culture with enough quantity to conquer the limitations using CEF cells and thus to vaccinate chicks to protect against IBDV infection.

Demonstration of receptor binding properties of VP2 of very virulent strain infectious bursal disease virus on Vero cells

2007 ◽  
Vol 123 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Chi Wai Yip ◽  
Yin Shan Yeung ◽  
Ching Man Ma ◽  
Pui Yi Lam ◽  
Chung Chau Hon ◽  
...  
Keyword(s):  
Disease Virus ◽  
Receptor Binding ◽  
Infectious Bursal Disease Virus ◽  
Virulent Strain ◽  
Vero Cells ◽  
Infectious Bursal Disease ◽  
Binding Properties ◽  
Bursal Disease

Small interfering RNAs inhibit infectious bursal disease virus replication in Vero cells

2011 ◽  
Vol 55 (1) ◽  
pp. 75-79 ◽  
Author(s):  
B. SAJJANAR ◽  
A. MISHRA ◽  
A. SONAWANE ◽  
C. PATEL ◽  
A. SAXENA ◽  
...  
Keyword(s):  
Disease Virus ◽  
Virus Replication ◽  
Infectious Bursal Disease Virus ◽  
Vero Cells ◽  
Infectious Bursal Disease ◽  
Small Interfering Rnas ◽  
Bursal Disease

scholarly journals Development of a Viral-Like Particle Candidate Vaccine Against Novel Variant Infectious Bursal Disease Virus

Vaccines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 142
Author(s):  
Yulong Wang ◽  
Nan Jiang ◽  
Linjin Fan ◽  
Li Gao ◽  
Kai Li ◽  
...  
Keyword(s):  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Protective Efficacy ◽  
Expression System ◽  
Size Exclusion ◽  
Candidate Vaccine ◽  
Infectious Bursal Disease ◽  
Immune Protection ◽  
Bursal Disease ◽  
Novel Variant

Infectious bursal disease (IBD), an immunosuppressive disease of young chickens, is caused by infectious bursal disease virus (IBDV). Novel variant IBDV (nVarIBDV), a virus that can evade immune protection against very virulent IBDV (vvIBDV), is becoming a threat to the poultry industry. Therefore, nVarIBDV-specific vaccine is much needed for nVarIBDV control. In this study, the VP2 protein of SHG19 (a representative strain of nVarIBDV) was successfully expressed using an Escherichia coli expression system and further purified via ammonium sulfate precipitation and size-exclusion chromatography. The purified protein SHG19-VP2-466 could self-assemble into 25-nm virus-like particle (VLP). Subsequently, the immunogenicity and protective effect of the SHG19-VLP vaccine were evaluated using animal experiments, which indicated that the SHG19-VLP vaccine elicited neutralization antibodies and provided 100% protection against the nVarIBDV. Furthermore, the protective efficacy of the SHG19-VLP vaccine against the vvIBDV was evaluated. Although the SHG19-VLP vaccine induced a comparatively lower vvIBDV-specific neutralization antibody titer, it provided good protection against the lethal vvIBDV. In summary, the SHG19-VLP candidate vaccine could provide complete immune protection against the homologous nVarIBDV as well as the heterologous vvIBDV. This study is of significance to the comprehensive prevention and control of the recent atypical IBD epidemic.

scholarly journals Chicken Heat Shock Protein 70 Is an Essential Host Protein for Infectious Bursal Disease Virus Infection In Vitro

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 664
Author(s):  
Yufang Meng ◽  
Xiaoxue Yu ◽  
Chunxue You ◽  
Wenjuan Zhang ◽  
Yingfeng Sun ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Disease Virus ◽  
Heat Shock Protein 70 ◽  
Infectious Bursal Disease Virus ◽  
Host Protein ◽  
Infectious Bursal Disease ◽  
Economic Losses ◽  
Small Interfering Rnas ◽  
Bursal Disease

Infectious bursal disease virus (IBDV) infection causes pathogenicity and mortality in chickens, leading to huge economic losses in the poultry industry worldwide. Studies of host-virus interaction can help us to better understand the viral pathogenicity. As a highly conservative host factor, heat shock protein 70 (Hsp70) is observed to be involved in numerous viral infections. However, there is little information about the role of chicken Hsp70 (cHsp70) in IBDV infection. In the present study, the increased expression of cHsp70 was observed during IBDV-infected DF-1 cells. Further studies revealed that Hsp70 had similar locations with the viral double-stranded RNA (dsRNA), and the result of pull-down assay showed the direct interaction between cHsp70 with dsRNA, viral proteins (vp)2 and 3, indicating that maybe cHsp70 participates in the formation of the replication and transcription complex. Furthermore, overexpression of cHsp70 promoted IBDV production and knockdown of cHsp70 using small interfering RNAs (siRNA) and reducedviral production, implying the necessity of cHsp70 in IBDV infection. These results reveal that cHsp70 is essential for IBDV infection in DF-1 cells, suggesting that targeting cHsp70 may be applied as an antiviral strategy.

scholarly journals Type I Interferon acts as a major barrier to the establishment of infectious bursal disease virus (IBDV) persistent infections

2020 ◽  
pp. JVI.02017-20
Author(s):  
Laura Broto ◽  
Nicolás Romero ◽  
Fernando Méndez ◽  
Elisabet Diaz-Beneitez ◽  
Oscar Candelas-Rivera ◽  
...  
Keyword(s):  
Disease Virus ◽  
Cell Lines ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Type I ◽  
Persistently Infected ◽  
Persistent Infections ◽  
Avian Pathogen ◽  
Bursal Disease ◽  
Infected Cells

Infectious bursal disease virus (IBDV), the best characterized member of the Birnaviridae family, is a highly relevant avian pathogen causing both acute and persistent infections in different avian hosts. Here, we describe the establishment of clonal, long-term, productive persistent IBDV infections in DF-1 chicken embryonic fibroblasts. Although virus yields in persistently-infected cells are exceedingly lower than those detected in acutely infected cells, the replication fitness of viruses isolated from persistently-infected cells is higher than that of the parental virus. Persistently-infected DF-1 and IBDV-cured cell lines derived from them do not respond to type I interferon (IFN). High-throughput genome sequencing revealed that this defect is due to mutations affecting the IFNα/β receptor subunit 2 (IFNAR2) gene resulting in the expression of IFNAR2 polypeptides harbouring large C-terminal deletions that abolish the signalling capacity of IFNα/β receptor complex. Ectopic expression of a recombinant chicken IFNAR2 gene efficiently rescues IFNα responsiveness. IBDV-cured cell lines derived from persistently infected cells exhibit a drastically enhanced susceptibility to establishing new persistent IBDV infections. Additionally, experiments carried out with human HeLa cells lacking the IFNAR2 gene fully recapitulate results obtained with DF-1 cells, exhibiting a highly enhanced capacity to both survive the acute IBDV infection phase and to support the establishment of persistent IBDV infections. Results presented here show that the inactivation of the JAK-STAT signalling pathway significantly reduces the apoptotic response induced by the infection, hence facilitating the establishment and maintenance of IBDV persistent infections.IMPORTANCE Members of the Birnaviridae family, including infectious bursal disease virus (IBDV), exhibit a dual behaviour, causing acute infections that are often followed by the establishment of life-long persistent asymptomatic infections. Indeed, persistently infected specimens might act as efficient virus reservoirs, hence potentially contributing to virus dissemination. Despite the key importance of this biological trait, information about mechanisms triggering IBDV persistency is negligible. Our report evidences the capacity of IBDV, a highly relevant avian pathogen, to establishing long-term, productive, persistent infections in both avian and human cell lines. Data presented here provide novel and direct evidence about the crucial role of type I IFNs on the fate of IBDV-infected cells and their contribution to controlling the establishment of IBDV persistent infections. The use of cell lines unable to respond to type I IFNs opens a promising venue to unveiling additional factors contributing to IBDV persistency.

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