Changes in the Cytokine and Toll-Like Receptor Gene Expression Following Infection of Indigenous and Commercial Chickens With Infectious bursal disease virus

Indigenous breeds of young chickens in India are believed to be resistant to the classical strain of infectious bursal disease virus (IBDV). However, the mechanism underlying this resistance is obscure. Innate immunity is a key factor in defining the clinical course and pathology of microbial infections. The present study is aimed to compare the pathology of very virulent IBDV (vvIBDV) and immunological host response in experimentally infected - vaccinated and unvaccinated indigenous Aseel and commercial White Leghorn chickens. The viral loads and innate immune gene expression profiles of MDA-5, Mx, IFN-α, and IFN-β in different lymphoid organs were analyzed by quantitative PCR. The histopathological scores in Aseel birds were lower than in White Leghorns despite comparable viral loads. The degrees of histopathological lesions were fewer in vaccinated birds than in unvaccinated birds of both breeds. Analysis of innate immune response genes revealed that the cytoplasmic pattern recognition receptor MDA-5 gene was overexpressed mainly in the cecal tonsils of both vaccinated and nonvaccinated White Leghorn chickens. An increase in the expression of the IFN-α gene was seen in the cecal tonsils of Aseels, and an increase in IFN-β gene expression was seen in the thymuses of White Leghorns following vvIBDV challenge both in vaccinated and nonvaccinated birds. In addition, we observed that the Mx gene plays a minimal role, if any, in vvIBDV infection of the breeds under study. It remains interesting and important that although vvIBDV causes disease in indigenous Aseel birds, the faster clearance and reduced pathology of the virus in Aseel birds compared to White Leghorn chicken indicate some unidentified innate immune factors that are limiting IBDV in this breed. Further studies will be required to correlate kinetics of humoral and cellular immune response in relation to the virus load in different organs to illuminate the mechanism of genetic resistance in native breeds of chicken.

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Analysis of the Early Immune Response to Infection by Infectious Bursal Disease Virus in Chickens Differing in Their Resistance to the Disease

Journal of Virology ◽

10.1128/jvi.02828-14 ◽

2014 ◽

Vol 89 (5) ◽

pp. 2469-2482 ◽

Cited By ~ 27

Author(s):

Jacqueline Smith ◽

Jean-Remy Sadeyen ◽

Colin Butter ◽

Pete Kaiser ◽

David W. Burt

Keyword(s):

Gene Expression ◽

Disease Virus ◽

Infectious Bursal Disease Virus ◽

Host Response ◽

Infectious Bursal Disease ◽

Expression Arrays ◽

Gene Expression Arrays ◽

Antiviral Genes ◽

Bursal Disease ◽

Comprehensive Study

ABSTRACTChicken whole-genome gene expression arrays were used to analyze the host response to infection by infectious bursal disease virus (IBDV). Spleen and bursal tissue were examined from control and infected birds at 2, 3, and 4 days postinfection from two lines that differ in their resistance to IBDV infection. The host response was evaluated over this period, and differences between susceptible and resistant chicken lines were examined. Antiviral genes, includingIFNA,IFNG,MX1,IFITM1,IFITM3, andIFITM5, were upregulated in response to infection. Evaluation of this gene expression data allowed us to predict several genes as candidates for involvement in resistance to IBDV.IMPORTANCEInfectious bursal disease (IBD) is of economic importance to the poultry industry and thus is also important for food security. Vaccines are available, but field strains of the virus are of increasing virulence. There is thus an urgent need to explore new control solutions, one of which would be to breed birds with greater resistance to IBD. This goal is perhaps uniquely achievable with poultry, of all farm animal species, since the genetics of 85% of the 60 billion chickens produced worldwide each year is under the control of essentially two breeding companies. In a comprehensive study, we attempt here to identify global transcriptomic differences in the target organ of the virus between chicken lines that differ in resistance and to predict candidate resistance genes.

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Effects of Chicken Anemia Virus and Infectious Bursal Disease Virus in Commercial Chickens

Avian Diseases ◽

10.1637/8408-071408-reg.1 ◽

2009 ◽

Vol 53 (1) ◽

pp. 94-102 ◽

Cited By ~ 17

Author(s):

H. Toro ◽

V. L. van Santen ◽

F. J. Hoerr ◽

C. Breedlove

Keyword(s):

Disease Virus ◽

Infectious Bursal Disease Virus ◽

Infectious Bursal Disease ◽

Chicken Anemia Virus ◽

Bursal Disease ◽

Anemia Virus ◽

Commercial Chickens

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The host genotype influences infectious bursal disease virus pathogenesis in chickens by modulation of T cells responses and cytokine gene expression

Developmental & Comparative Immunology ◽

10.1016/j.dci.2012.10.013 ◽

2013 ◽

Vol 40 (1) ◽

pp. 1-10 ◽

Cited By ~ 25

Author(s):

Merve Tippenhauer ◽

Dan E. Heller ◽

Steffen Weigend ◽

Silke Rautenschlein

Keyword(s):

Gene Expression ◽

T Cells ◽

Disease Virus ◽

Infectious Bursal Disease Virus ◽

Infectious Bursal Disease ◽

Cytokine Gene Expression ◽

Cytokine Gene ◽

Host Genotype ◽

Bursal Disease

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

10.1101/180158 ◽

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.

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