Immune Response and Pathogenicity of Different Strains of Infectious Bursal Disease Virus Applied as Vaccines

1978 ◽  
Vol 22 (4) ◽  
pp. 721 ◽  
Author(s):  
R. W. Winterfield ◽  
H. L. Thacker
Keyword(s):  
Immune Response ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Bursal Disease ◽  
Different Strains

scholarly journals A Comparative Study of Pathology and Host Immune Response Induced by Very Virulent Infectious Bursal Disease Virus in Experimentally Infected Chickens of Aseel and White Leghorn Breeds

Vaccines ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 627
Author(s):  
Shyama N. Prabhu ◽  
Ajay Pratap Singh ◽  
Berin P. Varghese ◽  
Kuldeep Dhama ◽  
Shambhu Dayal Singh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Innate Immune ◽  
Infectious Bursal Disease ◽  
White Leghorn ◽  
Viral Loads ◽  
White Leghorns ◽  
Bursal Disease

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.

scholarly journals Experimental co-infection of variant infectious bursal disease virus and fowl adenovirus serotype 4 increases mortality and reduces immune response in chickens

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
A-hui Xu ◽  
Lu Sun ◽  
Kai-hang Tu ◽  
Qing-yuan Teng ◽  
Jia Xue ◽  
...  
Keyword(s):  
Immune Response ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Clinical Symptoms ◽  
Interaction Mechanism ◽  
Infectious Bursal Disease ◽  
Adenovirus Serotype ◽  
Fowl Adenovirus ◽  
Bursal Disease ◽  
Fowl Adenovirus Serotype 4

AbstractInfectious bursal disease virus (IBDV) and fowl adenovirus serotype 4 (FAdV-4) cause infectious bursal disease (IBD) and hydropericardium-hepatitis syndrome, respectively. Recently, studies have reported co-infections of poultry with IBDV and FAdV-4, which is an important problem in the poultry industry. Here, the variant IBDV strain ZD-2018-1 and FAdV-4 isolate HB1501 were used to assess the pathogenicity of co-infection in 1-day-old specific pathogen-free (SPF) chickens. Compared with chickens infected with only FAdV-4, those coinfected with IBDV and FAdV-4 showed enhanced clinical symptoms, higher mortality, more severe tissue lesions, and higher biochemical index levels. Furthermore, the expression of interleukin (IL)-6, IL-1β, and interferon-γ mRNAs in the IBDV-FAdV-4 coinfected chickens was delayed, and the antibody response levels were significantly lower in those birds compared with the FAdV-4-infected chickens. These results indicate that co-infection with variant IBDV ZD-2018-1 and FAdV-4 HB1501 could significantly promote the pathogenicity of FAdV-4 and reduce the immune response in chickens. This study provides the foundation for further investigation of the interaction mechanism in IBDV and FAdV-4 co-infection.

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