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Updated: Jun 22, 2025

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Published on: October 17, 2012
Enterovirus-A71 exploits RAB11 to recruit chaperones for virus morphogenesis
Qing Yong Ng1,2, Vikneswari Mahendran1,2, Ze Qin Lim1,2
1Infectious Diseases Translational Research Programme, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Small GTPase RAB11A is a novel host factor in Enterovirus 71 (EV-A71) infection, aiding virus maturation by recruiting chaperone proteins. This finding reveals a new mechanism in EV-A71 pathogenesis and potential therapeutic targets.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Enterovirus 71 (EV-A71) causes Hand, Foot and Mouth Disease (HFMD) and neurological complications in children.
- The molecular mechanisms underlying EV-A71 pathogenesis are not fully understood.
Purpose of the Study:
- To identify host factors involved in EV-A71 pathogenesis.
- To elucidate the role of RAB11A in the EV-A71 life cycle.
Main Methods:
- siRNA screening of motor neurons infected with EV-A71.
- Validation of candidate genes, including RAB11A, using various molecular and imaging techniques.
- Mass spectrometry to identify RAB11A interacting partners.
Main Results:
- Small GTPase RAB11A was identified as a pro-viral host factor for EV-A71 and Coxsackievirus A16.
- RAB11A is crucial for provirion maturation, specifically VP0 cleavage.
- RAB11A interacts with chaperone proteins, including CCT8, to facilitate EV-A71 infection.
Conclusions:
- RAB11A plays an unconventional role in viral infection by mediating virus morphogenesis.
- Recruitment of chaperone proteins by RAB11A is essential for EV-A71 maturation.
- This study uncovers novel host-pathogen interactions in EV-A71 infection.
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