Immune response elicited by the oral administration of an intermediate strain of IBDV in chickens

Carballeda, Juan Manuel; Zoth, Silvina Andrea Chimeno; Gómez, Emma Laura Alfaro; Lucero, María Soledad; Gravisaco, Marí­a José; Berinstein, Analía

doi:10.1590/s1517-83822014000400049

Cited by 8 publications

(5 citation statements)

References 18 publications

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“…Perforin and granzyme-A dependant cytotoxic pathways of the cytotoxic T cell are mainly involved in the clearance of the IBDV from the BF, due to higher expression of these proteins in the CD4 and CD8 and BF cells (Rauf et al, 2011b). CD4 and CD8 cells populations appeared to increase in the BF, decrease in the thymus (particularly in the cortex), and show an increasing trend for CD4 and decreasing CD8, which was observed in the spleen in vvIBDV infected chickens (Carballeda et al, 2014), although results from work by Rodenberg et al (1994) were contradictory. It is not clear whether these higher populations are due to cell migration from the tissues to the periphery or contractions of the resident cells (Rasoli et al, 2015).…”

Section: Cd4 and Cd8 Cellsmentioning

confidence: 95%

“…IBDV infection in chicken promotes the expression of the pro-inflammatory cytokines and chemokines, Th1 cytokines, iNOS and MHC class I in HD11 cells in vitro (Rasoli et al, 2015) and upregulate chicken IL-12 and IL-18 in HD11 cells infected with IBDV (Khatri et al, 2005;Lee et al, 2015b). IBDV also upregulates the IL-6, IL-8 and interferons (IFNs) expression in the BF (Carballeda et al, 2014) and IL-8 (Rauf et al, 2011a). Temporary up regulation of IFN-γ, IL-2, IL-6 and down regulation of the cytokine IL-1β and type IIFNs were noted in IBDV infection (Rautenschlein et al, 2007;Eldaghayes et al, 2006).…”

Section: Cytokines and Chemokinesmentioning

confidence: 99%

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Interaction of infectious bursal disease virus with the immune system of poultry

Rehman

Chen

Umar

et al. 2016

World's Poultry Science Journal

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Immune dysfunction can be either at the humoral or cellular levels and is mediated by a myriad of factors including virus-induced immunosuppression. Infectious bursal disease virus (IBDV) affects domesticated poultry and causing health problems mainly due to prolonged immunosuppression. Destruction of the immunoglobulin-producing cells is the principal cause of IBDV-induced immunosuppression, which leads to significant impairment of the primary antibody responses. Due to these effects, IBDV infection not only increases the susceptibility of poultry to other viral infections but predisposes the host to several other bacteria of variable pathologies. The IBDV-induced immunesuppression is well-known phenomenon, however, recently there have been significant advancements in understanding the molecular mechanisms of this immune-suppression. This review discuss current updates regarding the immunotoxic and immunosuppressive nature of IBDV in the poultry and highlights areas requiring future research attentions that may help to establish foundations for effective and improved vaccines against IBDV.

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Section: Cd4 and Cd8 Cellsmentioning

confidence: 95%

Section: Cytokines and Chemokinesmentioning

confidence: 99%

Interaction of infectious bursal disease virus with the immune system of poultry

Rehman

Chen

Umar

et al. 2016

World's Poultry Science Journal

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“…RNA was extracted from BF samples and reverse transcribed to cDNA that was used as the template in qPCR assays targeting chicken type I IFN genes IFNα, IFNβ and Mx1, and pro-inflammatory cytokines IL-6, IL-8, and IL-1β. These genes were selected as they are the most relevant to studying antiviral type I IFN and pro-inflammatory responses, and have previously been shown to be upregulated following IBDV infection (Guo et al, 2012;Carballeda et al, 2014;Giotis et al, 2017;Quan et al, 2017;He et al, 2018). The mean expression of IFNα (Figure 2A), IFNβ ( Figure 2B), and Mx1 ( Figure 2C) was lower in BF samples harvested from UK661infected birds compared to F52/70-infected birds at 24 and 48 h post-inoculation, which was statistically significant for IFNβ at 48 hpi and Mx1 at 24, 48, and 72 hpi ( * P < 0.05).…”

Section: Resultsmentioning

confidence: 99%

“…The IFN response aims to provide an antiviral state in infected and bystander cells. In addition, pro-inflammatory cytokines, for example IL-6, IL-8, and IL-1β are produced following IBDV infection that recruit immune cells into the infected BF (Guo et al, 2012;Carballeda et al, 2014;Quan et al, 2017;He et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

The Stronger Downregulation of in vitro and in vivo Innate Antiviral Responses by a Very Virulent Strain of Infectious Bursal Disease Virus (IBDV), Compared to a Classical Strain, Is Mediated, in Part, by the VP4 Protein

Dulwich

Asfor

Gray

et al. 2020

Front. Cell. Infect. Microbiol.

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IBDV is economically important to the poultry industry. Very virulent (vv) strains cause higher mortality rates than other strains for reasons that remain poorly understood. In order to provide more information on IBDV disease outcome, groups of chickens (n = 18) were inoculated with the vv strain, UK661, or the classical strain, F52/70. Birds infected with UK661 had a lower survival rate (50%) compared to F52/70 (80%). There was no difference in peak viral replication in the bursa of Fabricius (BF), but the expression of chicken IFNα, IFNβ, MX1, and IL-8 was significantly lower in the BF of birds infected with UK661 compared to F52/70 (p < 0.05) as quantified by RTqPCR, and this trend was also observed in DT40 cells infected with UK661 or F52/70 (p < 0.05). The induction of expression of type I IFN in DF-1 cells stimulated with polyI:C (measured by an IFN-β luciferase reporter assay) was significantly reduced in cells expressing ectopic VP4 from UK661 (p < 0.05), but was higher in cells expressing ectopic VP4 from F52/70. Cells infected with a chimeric recombinant IBDV carrying the UK661-VP4 gene in the background of PBG98, an attenuated vaccine strain that induces high levels of innate responses (PBG98-VP4 UK661) also showed a reduced level of IFNα and IL-8 compared to cells infected with a chimeric virus carrying the F52/70-VP4 gene (PBG98-VP4 F52/70) (p < 0.01), and birds infected with PBG98-VP4 UK661 also had a reduced expression of IFNα in the BF compared to birds infected with PBG98-VP4 F52/70 (p < 0.05). Taken together, these data demonstrate that UK661 induced the expression of lower levels of anti-viral type I IFN and proinflammatory genes than the classical strain in vitro and in vivo and this was, in part, due to strain-dependent differences in the VP4 protein.

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“…The IFN-response aims to provide an antiviral state in infected and bystander cells. In addition, pro-inflammatory cytokines, for example IL-6, IL-8 and IL-1β are produced following IBDV infection that recruit immune cells into the infected bursa of Fabricius (BF) [12–15].…”

Section: Introductionmentioning

confidence: 99%

The stronger downregulation ofin vitroandin vivoinnate antiviral responses by a very virulent strain of infectious bursal disease virus (IBDV), compared to a classical strain, is mediated, in part, by the VP4 protein

Dulwich

Asfor

Gray

et al. 2019

Preprint

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word count: 279 14 15 Text word Count: 5,698 16 17 Abstract 18IBDV is economically important to the poultry industry. Very virulent (vv) strains cause higher 19 mortality rates than other strains for reasons that remain poorly understood. In order to provide 20 more information on IBDV disease outcome, groups of chickens (n=18) were inoculated with the vv 21 strain, UK661, or the classical strain, F52/70. Birds infected with UK661 had a lower survival rate 22 (50%) compared to F52/70 (80%). There was no difference in peak viral replication in the bursa of 23 Fabricius (BF), but the expression of chicken IFNβ, MX1 and IL-8 was significantly lower in the BF of 24 birds infected with UK661 compared to F52/70 (p<0.05) as quantified by RTqPCR, and this trend was 25 also observed in DT40 cells infected with UK661 or F52/70 (p<0.05). The induction of expression of 26 in vivo and this was, in part, due to strain-dependent differences in the VP4 protein. 36 37 39 (c) strains have circulated worldwide, however, in the 1980s, so-called "very virulent" (vv) strains 53 emerged, complicating IBDV control efforts [6, 7]. The vvIBDV strains cause a far higher mortality 54 rate than classical strains, reaching up to 60-70% in some flocks [8]. However, the molecular basis for 55 the difference in disease outcome remains poorly understood, although it has been demonstrated 56 that both segments A and B contribute to virulence [9]. Segment A encodes the non-structural 57 protein, VP5, and a polyprotein (VP2-VP4-VP3) which is co-translationally cleaved by the protease, 58 VP4 [10]. VP2 is the capsid protein and VP3 is a multifunctional scaffolding protein that binds the 59 genome. The single ORF on Segment B encodes VP1, the RNA-dependent RNA polymerase. 60 61The innate immune response to IBDV infection is characterised by the production of type I IFN 62responses, including the upregulation of IFNα and IFNβ, that lead to the induction of interferon 63 stimulated genes (ISGs), including MX1, which is one of the top ISGs identified in chicken cells ranked 64 by fold change [11]. The IFN-response aims to provide an antiviral state in infected and bystander 65 cells. In addition, pro-inflammatory cytokines, for example IL-6, IL-8 and IL-1β are produced 66 following IBDV infection that recruit immune cells into the infected bursa of Fabricius (BF) [12][13][14][15]. 67 68We sought to identify IBDV virulence determinants in order to better understand the molecular basis 69 of phenotypic differences between vv-and c-IBDV strains. Here we report that vvIBDV UK661 down-70 regulated the expression of antiviral type I IFN responses and pro-inflammatory cytokines compared 71 to cIBDV F52/70 in vitro and in vivo. Moreover, we demonstrate that the differences in IFN 72 antagonism were, in part, due to strain-dependent differences in the VP4 proteins. 73 74 Materials and methods 75 76 Cells and viruses. DF-1 cells (chicken embryonic fibroblast cells, ATCC number CRL-12203) were 77 sustained in Dulbecco's modified Eagle's medium (DMEM) (Sigma-Aldrich...

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Immune response elicited by the oral administration of an intermediate strain of IBDV in chickens

Cited by 8 publications

References 18 publications

Interaction of infectious bursal disease virus with the immune system of poultry

Interaction of infectious bursal disease virus with the immune system of poultry

The Stronger Downregulation of in vitro and in vivo Innate Antiviral Responses by a Very Virulent Strain of Infectious Bursal Disease Virus (IBDV), Compared to a Classical Strain, Is Mediated, in Part, by the VP4 Protein

The stronger downregulation ofin vitroandin vivoinnate antiviral responses by a very virulent strain of infectious bursal disease virus (IBDV), compared to a classical strain, is mediated, in part, by the VP4 protein

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