Viral protein responsible for IBDV virulence
IBDV protein that dampens poultry immune response could inform vaccine development.
June 29, 2020
Research carried out by scientists at The Pirbright Institute in the U.K. has revealed that differences in virulence between strains of infectious bursal disease virus (IBDV) may be partly due to changes in a viral protein called VP4.
The findings could help scientists understand why very virulent (vv) strains cause high mortality rates in some commercial poultry flocks and could also be used to inform vaccine research and surveillance efforts, Pirbright said in its announcement.
IBDV is among the top five infectious problems of chickens and poses a continuous threat to the poultry industry though economic losses and welfare concerns. The virus infects cells of the immune system, meaning surviving birds are often more susceptible to secondary infections and less responsive to vaccination programs, the institute said.
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, but the reason for this is still poorly understood.
In the study, published in Frontiers in Cellular & Infection Microbiology, the team compared a vv strain of IBDV to a less-virulent classical field strain 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, 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,” Dr. Andrew Broadbent, head of the Birnavirus Group at Pirbright, said.
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, Pirbright said. 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.
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