IBDV VP4 protein dampens poultry immune response
Work carried out by scientists at The Pirbright Institute has revealed that differences in virulence between strains of Infectious bursal disease virus (IBDV) may be partly down to changes in the VP4 protein. Their findings, published in Frontiers in Cellular and Infection Microbiology, may help explain why very virulent (vv) strains cause high mortality rates in some commercial poultry flocks.
IBDV infects cells of the immune system; surviving birds are often more susceptible to secondary infections and less responsive to vaccination programmes. The vv strains of IBDV emerged in the 1980s and Pirbright researchers were the first to sequence their genome. These strains were more deadly than classical strains, however the reason for this is still poorly understood.
The team compared a vv strain (UK661) of IBDV to a less virulent classical field strain (F52/70) and found that the vv IBDV inhibited the antiviral response of infected cells more than the classical strain. The researchers found that this was partly due to genetic variations in the VP4 protein, suggesting that the VP4 protein might contribute to IBDV virulence.
Dr Andrew Broadbent, Head of the Birnavirus Group at Pirbright said: “We saw higher levels of vv IBDV replication in cells than the classical strain, so it is possible that by preventing this antiviral response, the vv strains are able to replicate more efficiently, which gives them an advantage over the classical strains and encourages their spread and evolution”.
The researchers say that further exploration of the VP4 protein could prove useful for IBDV vaccine development, as the VP4 gene from less virulent strains could be inserted into vv strains to weaken them for use in vaccines. The new information from this study could also be used to improve IBDV surveillance efforts and control strategies. For example, understanding the genetic signatures that increase the virulence of IBDV strains could be used to better inform national surveillance efforts in order to assess the potential threat of an emerging strain as early as possible.
Article: Dulwich, K.L., Asfor, A., Gray, A., Giotis, E.S., Skinner, M.A., Broadbent, A.J. (2020) 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. Frontiers in Cellular and Infection Microbiology, 10:315, doi: 10.3389/fcimb.2020.00315
[SOURCE: The Pirbright Institute]