Abrogation of attachment of Infectious Bursal Disease Virus to chicken B cells by treatment of B cells with Soyabean Agglutinin and Wheat Germ Lectin

10.5580/1c42 ◽  
2008 ◽  
Vol 6 (2) ◽  
Keyword(s):  
B Cells ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Wheat Germ ◽  
Infectious Bursal Disease ◽  
Bursal Disease ◽  
Wheat Germ Lectin

scholarly journals Identification of Chicken CD74 as a Novel Cellular Attachment Receptor for Infectious Bursal Disease Virus in Bursa B Lymphocytes

2019 ◽  
Vol 94 (2) ◽  
Author(s):  
Aijing Liu ◽  
Qing Pan ◽  
Yue Li ◽  
Nana Yan ◽  
Jing Wang ◽  
...  
Keyword(s):  
B Cells ◽  
Cell Line ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
B Lymphocyte ◽  
Pivotal Role ◽  
Infectious Bursal Disease ◽  
Antigenic Peptides ◽  
Bursal Disease

ABSTRACT Infectious bursal disease virus (IBDV) is an important member of the Birnaviridae family, causing severe immunosuppressive disease in chickens. The major capsid protein VP2 is responsible for the binding of IBDV to the host cell and its cellular tropism. In order to find proteins that potentially interact with IBDV VP2, a liquid chromatography-mass spectrometry (LC-MS) assay was conducted, and the host chicken CD74 protein was identified. Here, we investigate the role of chicken CD74 in IBDV attachment. Coimmunoprecipitation assays indicated that the extracellular domain of CD74 interacted with the VP2 proteins of multiple IBDV strains. Knockdown and overexpression experiments showed that CD74 promotes viral infectivity. Confocal assays showed that CD74 overexpression allows the attachment of IBDV and subvirus-like particles (SVPs) to the cell surface of nonpermissive cells, and quantitative PCR (qPCR) analysis further confirmed the attachment function of CD74. Anti-CD74 antibody, soluble CD74, depletion of CD74 by small interfering RNA (siRNA), and CD74 knockdown in the IBDV-susceptible DT40 cell line significantly inhibited IBDV binding, suggesting a pivotal role of this protein in virus attachment. These findings demonstrate that CD74 is a novel important receptor for IBDV attachment to the chicken B lymphocyte cell line DT40. IMPORTANCE CD74 plays a pivotal role in the correct folding and functional stability of major histocompatibility complex class II (MHC-II) molecules and in the presentation of antigenic peptides, acting as a regulatory factor in the antigen presentation process. In our study, we demonstrate a novel role of CD74 during IBDV infection, showing that chicken CD74 plays a significant role in IBDV binding to target B cells by interacting with the viral VP2 protein. This is the first report demonstrating that CD74 is involved as a novel attachment receptor in the IBDV life cycle in target B cells, thus contributing new insight into host-pathogen interactions.

scholarly journals Genome Evolution of Two Genetically Homogeneous Infectious Bursal Disease Virus Strains During Passages in vitro and ex vivo in the Presence of a Mutagenic Nucleoside Analog

2021 ◽  
Vol 12 ◽  
Author(s):  
Liliana L. Cubas-Gaona ◽  
Alexandre Flageul ◽  
Céline Courtillon ◽  
Francois-Xavier Briand ◽  
Maud Contrant ◽  
...  
Keyword(s):  
B Cells ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Virulent Strain ◽  
Nucleoside Analog ◽  
Viral Fitness ◽  
Infectious Bursal Disease ◽  
Selection Pressures ◽  
Bursal Disease

The avibirnavirus infectious bursal disease virus (IBDV) is responsible for a highly contagious and sometimes lethal disease of chickens (Gallus gallus). IBDV genetic variation is well-described for both field and live-attenuated vaccine strains, however, the dynamics and selection pressures behind this genetic evolution remain poorly documented. Here, genetically homogeneous virus stocks were generated using reverse genetics for a very virulent strain, rvv, and a vaccine-related strain, rCu-1. These viruses were serially passaged at controlled multiplicities of infection in several biological systems, including primary chickens B cells, the main cell type targeted by IBDV in vivo. Passages were also performed in the absence or presence of a strong selective pressure using the antiviral nucleoside analog 7-deaza-2′-C-methyladenosine (7DMA). Next Generation Sequencing (NGS) of viral genomes after the last passage in each biological system revealed that (i) a higher viral diversity was generated in segment A than in segment B, regardless 7DMA treatment and viral strain, (ii) diversity in segment B was increased by 7DMA treatment in both viruses, (iii) passaging of IBDV in primary chicken B cells, regardless of 7DMA treatment, did not select cell-culture adapted variants of rvv, preserving its capsid protein (VP2) properties, (iv) mutations in coding and non-coding regions of rCu-1 segment A could potentially associate to higher viral fitness, and (v) a specific selection, upon 7DMA addition, of a Thr329Ala substitution occurred in the viral polymerase VP1. The latter change, together with Ala270Thr change in VP2, proved to be associated with viral attenuation in vivo. These results identify genome sequences that are important for IBDV evolution in response to selection pressures. Such information will help tailor better strategies for controlling IBDV infection in chickens.

scholarly journals Differential gene expression in chicken primary B cells infected ex vivo with attenuated and very virulent strains of infectious bursal disease virus (IBDV)

2017 ◽  
Author(s):  
Katherine L. Dulwich ◽  
Efstathios S. Giotis ◽  
Alice Gray ◽  
Venugopal Nair ◽  
Michael A. Skinner ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cells ◽  
B Cell ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Ex Vivo ◽  
Lymphoid Cells ◽  
Infectious Bursal Disease ◽  
Type I ◽  
Bursal Disease

AbstractInfectious bursal disease virus (IBDV) belongs to the family Birnaviridae and is economically important to the poultry industry worldwide. IBDV infects B cells in the bursa of Fabricius (BF), causing immunosuppression and morbidity in young chickens. In addition to strains that cause classical Gumboro disease, the so-called ‘very virulent’ (vv) strain, also in circulation, causes more severe disease and increased mortality. IBDV has traditionally been controlled through the use of live attenuated vaccines, with attenuation resulting from serial passage in non-lymphoid cells. However, the factors that contribute to the vv or attenuated phenotypes are poorly understood. In order to address this, we aimed to investigate host cell-IBDV interactions using a recently described chicken primary B cell model, where chicken B cells are harvested from the BF and cultured ex vivo in the presence of chicken CD40L. We demonstrated that these cells could support the replication of IBDV when infected ex vivo in the laboratory. Furthermore, we evaluated the gene expression profiles of B cells infected with an attenuated strain (D78) and a very virulent strain (UK661) by microarray. We found that key genes involved in B cell activation and signaling (TNFSF13B, CD72 and GRAP) were down-regulated following infection relative to mock, which we speculate could contribute to IBDV-mediated immunosuppression. Moreover, cells responded to infection by expressing antiviral type I IFNs and IFN-stimulated genes, but the induction was far less pronounced upon infection with UK661, which we speculate could contribute to its virulence.

Infectious bursal disease virus (IBDV) induces apoptosis in chicken B cells

2005 ◽  
Vol 28 (4) ◽  
pp. 321-337 ◽  
Author(s):  
Juan Carlos Rodríguez-Lecompte ◽  
Rodolfo Niño-Fong ◽  
Alfonso Lopez ◽  
R.J. Frederick Markham ◽  
Frederick S.B. Kibenge
Keyword(s):  
B Cells ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease

scholarly journals Characteristics of Bursal T Lymphocytes Induced by Infectious Bursal Disease Virus

2000 ◽  
Vol 74 (19) ◽  
pp. 8884-8892 ◽  
Author(s):  
In-Jeong Kim ◽  
Seung Kwon You ◽  
Hyungee Kim ◽  
Hung-Yeuh Yeh ◽  
Jagdev M. Sharma
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
T Lymphocytes ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Dependent Manner ◽  
Bursal Disease

ABSTRACT Infectious bursal disease virus (IBDV) is an avian lymphotropic virus that causes immunosuppression. When specific-pathogen-free chickens were exposed to a pathogenic strain of IBDV (IM), the virus rapidly destroyed B cells in the bursa of Fabricius. Extensive viral replication was accompanied by an infiltration of T cells in the bursa. We studied the characteristics of intrabursal T lymphocytes in IBDV-infected chickens and examined whether T cells were involved in virus clearance. Flow cytometric analysis of single-cell suspensions of the bursal tissue revealed that T cells were first detectable at 4 days postinoculation (p.i.). At 7 days p.i., 65% of bursal cells were T cells and 7% were B cells. After virus infection, the numbers of bursal T cells expressing activation markers Ia and CD25 were significantly increased (P < 0.03). In addition, IBDV-induced bursal T cells produced elevated levels of interleukin-6-like factor and nitric oxide-inducing factor in vitro. Spleen and bursal cells of IBDV-infected chickens had upregulated gamma interferon gene expression in comparison with virus-free chickens. In IBDV-infected chickens, bursal T cells proliferated in vitro upon stimulation with purified IBDV in a dose-dependent manner (P < 0.02), whereas virus-specific T-cell expansion was not detected in the spleen. Cyclosporin A treatment, which reduced the number of circulating T cells and compromised T-cell mitogenesis, increased viral burden in the bursae of IBDV-infected chickens. The results suggest that intrabursal T cells and T-cell-mediated responses may be important in viral clearance and promoting recovery from infection.

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.

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