Ma ST(1)(2), Wang YS(1)(2), Wang XL(1)(2), Xia XX(1)(2), Bi ZW(1)(2), Wang JY(1)(2), Zhu YM(1)(2), Ouyang W(3)(4), Qian J(5)(6). Author information:
(1)Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences,
Nanjing, 210014, China.
(2)Key Laboratory for Veterinary Bio-Product Engineering, Ministry of
Agriculture, Nanjing, 210014, China.
(3)Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences,
Nanjing, 210014, China. [Email]
(4)Key Laboratory for Veterinary Bio-Product Engineering, Ministry of
Agriculture, Nanjing, 210014, China. [Email]
(5)Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences,
Nanjing, 210014, China. [Email]
(6)Key Laboratory for Veterinary Bio-Product Engineering, Ministry of
Agriculture, Nanjing, 210014, China. [Email]
The structural protein VP3 of infectious bursal disease virus (IBDV) plays a critical role in viral assembly, replication, immune escape, and anti-apoptosis. Interaction between VP3 and host protein factors can affect stages in the viral replication cycle. In this study, 137 host proteins interacting with VP3 protein were screened through liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomics approach. The functions and relevance of the proteins were obtained through bioinformatics analysis. Most VP3-interacting proteins were linked to binding, catalytic activity, and structural molecular activity, and performed functions in cell parts and cells. Biological functions of VP3-interacting proteins were mainly relevant to "Cytoskeleton", "Translation", and "Signal transduction mechanisms", involving ribosomes, "Tight junction", regulation of actin cytoskeleton, and other pathways. Six potential VP3-interacting proteins in host cells were knocked down, and vimentin, myosin-9, and annexin A2 were found to be related to IBDV replication. This study would help explore regulatory pathways and cellular mechanisms in IBDV-infected cells, and also provided clues for the in-depth study of VP3 biological functions and IBDV replication or pathogenesis.
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