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Long Non-Coding RNA NEAT1 Inhibits Enterovirus 71 Replication by Enhancing IFN-β Transcription Through DDX60
Dong Li1, Shuaiyin Chen1, Wangquan Ji1
1Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.
The Journal of Infectious Diseases
|November 12, 2025
Summary
Enterovirus 71 (EV71) infection increases NEAT1, which enhances interferon-beta (IFN-β) production to fight the virus. Lower NEAT1 levels in hand, foot, and mouth disease (HFMD) patients indicate a poorer prognosis.
Area of Science:
- Molecular Biology
- Immunology
- Virology
Background:
- Enterovirus 71 (EV71) causes severe hand, foot, and mouth disease (HFMD), but its pathogenesis is unclear.
- Understanding host responses to EV71 is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of NEAT1 in EV71 infection and host defense.
- To elucidate the molecular mechanisms by which NEAT1 influences EV71 pathogenesis.
Main Methods:
- EV71 infection models in vitro and in vivo.
- Analysis of NEAT1 and paraspeckle formation.
- Investigation of the DDX60-IRF7 pathway and IFN-β transcription.
- Case-control study correlating NEAT1 levels with HFMD severity.
Main Results:
- EV71 infection upregulates NEAT1, leading to paraspeckle formation.
- NEAT1 enhances IFN-β transcription via the DDX60-IRF7 pathway, promoting anti-EV71 resistance.
- NEAT1 facilitates SFPQ relocation, relieving transcriptional repression on DDX60 and MDA5.
- Reduced NEAT1-2 expression in HFMD patients correlates with disease severity.
Conclusions:
- NEAT1 acts as an intrinsic antiviral molecule against EV71.
- NEAT1-mediated IFN-β production is a key host defense mechanism against EV71.
- Low NEAT1 levels may predict a poor prognosis in HFMD patients.
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