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Interaction Network Characterization of Infectious Bronchitis Virus Nsp2 with Host Proteins
Mengmeng Wang1, Zongyi Bo1,2, Chengcheng Zhang1
1Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
Veterinary Sciences
|November 26, 2024
Summary
This study identifies host proteins interacting with the Infectious Bronchitis Virus (IBV) Nsp2 protein, revealing their roles in viral pathogenesis and replication. Findings highlight Nsp2
Area of Science:
- Veterinary Virology
- Molecular Pathogenesis
- Poultry Health
Background:
- Infectious Bronchitis Virus (IBV) causes significant economic losses in poultry.
- The Nsp2 protein is a potential key virulence factor in IBV, but its host interactions are poorly understood.
Purpose of the Study:
- To identify and characterize host proteins that interact with the IBV Nsp2 protein.
- To elucidate the role of these interactions in IBV pathogenesis and viral replication.
Main Methods:
- Yeast two-hybrid screening and molecular docking simulations to identify potential interacting proteins.
- Co-immunoprecipitation and confocal microscopy to validate interactions.
- Gene Ontology (GO), KEGG, and Protein-Protein Interaction (PPI) database analysis.
- Analysis of host protein expression levels during IBV infection.
Main Results:
- Ten host proteins (COX1, COX3, NFIA, ITGA1, ATP1B1, ATP1B3, ABCB1, ISCA1, DNAJA1, IREB2) were identified as potential interactors of IBV Nsp2.
- Interactions with ATP1B3, DNAJA1, and ISCA1 were validated.
- Interacting proteins are involved in ATPase activation, Fe-S cluster binding, ion homeostasis, and innate immunity.
- IBV infection altered the expression of host proteins, with downregulation of COX3, COX1, ATP1B1, ATP1B3 and upregulation of NFIA, DNAJA1, IREB2.
- IBV upregulates DNAJA1 expression, potentially enhancing viral replication.
Conclusions:
- The IBV Nsp2 protein interacts with multiple host proteins involved in critical cellular functions.
- These interactions likely contribute to IBV pathogenesis and viral proliferation.
- Upregulation of DNAJA1 by IBV may be a mechanism to enhance viral replication, warranting further investigation.
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