Infectious Bursal Disease Virus-Host Interactions: Multifunctional Viral Proteins that Perform Multiple and Differing Jobs - PubMed
- ️Sun Jan 01 2017
Review
Infectious Bursal Disease Virus-Host Interactions: Multifunctional Viral Proteins that Perform Multiple and Differing Jobs
Yao Qin et al. Int J Mol Sci. 2017.
Abstract
Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive poultry disease caused by IBD virus (IBDV). The consequent immunosuppression increases susceptibility to other infectious diseases and the risk of subsequent vaccination failure as well. Since the genome of IBDV is relatively small, it has a limited number of proteins inhibiting the cellular antiviral responses and acting as destroyers to the host defense system. Thus, these virulence factors must be multifunctional in order to complete the viral replication cycle in a host cell. Insights into the roles of these viral proteins along with their multiple cellular targets in different pathways will give rise to a rational design for safer and effective vaccines. Here we summarize the recent findings that focus on the virus-cell interactions during IBDV infection at the protein level.
Keywords: cellular target; immunosuppression; infectious bursal disease virus (IBDV).
Conflict of interest statement
The authors declare no conflict of interest. The founding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.
Figures

Schematic illustration of apoptosis and immunosuppression induced by viral proteins via interaction with cellular targets; Once expressed inside host cells, the viral proteins of IBDV, via interaction with cellular targets, play different roles in facilitation of IBDV replication; NF-kB: nuclear factor kappa enhancer binding protein; JNK: c-Jun-N-terminal kinase; AP-1: activating protein-1; IRF: interferon regulatory factor; PI3K: phosphoinositol-3 kinase; MAVS: mitochondrial antiviral signaling protein; CARD: caspase activation and recruitment domain; eif: eukaryotic initiation factor; ORAOV1: oral cancer overexpressed 1; GILZ: glucocorticoid-induced leucine zipper; VDAC2: voltage-dependent anion channel 2; RACK1: receptor of activated protein kinase C1; IFN: interferon; Cyto-C: cytochrome c; Casp: caspase; dsRNA: double-stranded RNA.
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