Research Advances the Understanding of Vaccination against Arkansas Infectious Bronchitis30 November 2013
Auburn University research has shed new light on continued outbreaks of Infectious Bronchitis in the US despite widespread vaccination. It appears that there have been mutations in the field strain of the virus that enable it to 'escape' the chicken's immune response.
Recurrent outbreaks of Ark-serotype infectious bronchitis virus (IBV) occur in spite of widespread vaccination, according to F.W. van Ginkel, Haroldo Toro and Vicky L van Santen of Auburn University.
They explain that the part of the IBV that the chicken's immune system recognises and responds to by producing a protective immune response is called the S1 protein. This protein often changes slightly as the virus replicates in birds, resulting in small but important changes in the S1 protein. These small changes are thought to allow the virus to escape from the immune response of the chicken.
Chickens produce two types of antibody in response to IBV vaccination - IgA which is secreted onto the mucosal surfaces of the eyes and upper respiratory tract (mucosal immunity) and IgG, which circulates systemically in the bloodstream (humoral immunity).
In this research project, sponsored by the US Poultry & Egg Association, several ARK S1 proteins with slight differences were used to immunise chickens. The genes for these S1 proteins were inserted into an adenovirus (Ad5) and the adenovirus, which expressed the S1 protein, was then used as the vaccine. The dynamics of the immune response to the different S1 proteins were studied.
The Auburn researchers outlined the objectives of their study as:
- To characterise B cell responses in head-associated lymphoid tissue (HALT) [Harderian glands and conjunctiva-associated lymphoid tissue (CALT)] and spleen after immunisation with Ad5 expressing distinct IBV Ark S1 genes and determine how these responses correlate with resistance to IBV challenge, and
- To characterise IBV-specific T cell responses in HALT and spleen in chickens after immunisation with Ad5 expressing distinct IBV Ark S1 proteins.
The research has made great strides in better understanding the T and B cell response to IBV in both the systemic and mucosal immune compartment, van Ginkel and colleagues noted.
The data indicate that mucosal immunity is important in the primary immune response but that the memory response seems to be dominated by central memory T cells.
The IBV-specific primary immune response is dominated by humoral and cell-mediated immunity in mucosa-associated lymphoid tissues while a subsequent IBV response is characterised by a systemic immune compartment dominated immune response. Thus, IBV boosting induces a central memory T cell response and an IgG dominated humoral immune response.
Furthermore, they report, there seems to be a functional divergence in the head-associated lymphoid tissues. The Harderian glands are more prone to generate humoral immunity to IBV, while the conjunctiva-associated lymphoid tissue seems more geared to cell-mediated immunity. The peptide arrays use for humoral immune responses the Ad5-C2 and IBV indicate that linear B cell epitopes are predominantly recognised by IgA antibodies while IgG antibodies are more prone to recognise conformational epitopes.
Point mutations in a field strain of IBV in the S1 part of the spike protein in B cell epitopes recognised by IgA reduces immune recognition of these epitopes by IgA antibodies when compared with the response to these epitopes to the vaccine strain. This indicates that these point mutations help the field strain to escape the mucosal IgA response.
The Auburn data is consistent with the importance of mucosal IgA in the protection against IBV, say the researchers.
Based on these observations, van Ginkle and colleagues conclude it seems important for IBV vaccines to induce and maintain IBV-specific mucosal immunity. In addition, selection of a recombinant expressed gene for induction of immunity can be tricky, as is exemplified by the best protection observed by Ad5-C2, while the Ad5-C4, with just one amino acid different, provided the worst protection upon IBV challenge.
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