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Analysis of EV71 infection progression using triple-SILAC-based proteomics approach
Hao-Yu Li1,2, Lei-Ke Zhang3, Xiu-Juan Zhu1,2
1State Key Laboratory of Virology, Wuhan University, Wuhan, P. R. China.
Proteomics
|August 27, 2015
Summary
Enterovirus 71 (EV71) infection alters host cell proteins, revealing CHCH2 as a key regulator. This mitochondrial protein negatively impacts innate immunity and EV71 replication.
Area of Science:
- Virology
- Proteomics
- Immunology
Background:
- Enterovirus 71 (EV71) causes severe neurological and systemic diseases in children.
- Understanding virus-host interactions is crucial for developing antiviral strategies.
Purpose of the Study:
- To investigate host cell proteome alterations during EV71 infection using quantitative proteomics.
- To identify host factors involved in EV71 replication and innate immune response.
Main Methods:
- Triple-SILAC (Stable Isotope Labeling by Amino acids in Cell culture) quantitative proteomics was employed.
- Over 4100 host proteins were quantified at 8 and 20 hours post-EV71 infection.
- Functional screening was performed on significantly regulated proteins.
Main Results:
- Approximately 17% of quantified proteins showed significant changes (p<0.01) post-infection.
- Five biological processes and seven protein classes were significantly affected.
- CHCH2, a mitochondrial protein, was identified as a regulator of EV71 replication and a negative regulator of innate immunity.
Conclusions:
- EV71 infection induces substantial changes in the host cell proteome.
- CHCH2 plays a critical role in modulating both viral replication and the host's innate immune defense against EV71.
- These findings provide insights into EV71 pathogenesis and potential therapeutic targets.
