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Updated: Jan 22, 2026
10:01
Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
Published on: October 17, 2018
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Interplay between Zika Virus and Peroxisomes during Infection
Cheung Pang Wong1, Zaikun Xu2, Shangmei Hou2
1Department of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, Canada.
Cells
|July 18, 2019
Summary
Zika virus depletes peroxisomes in brain cells, impairing antiviral defenses. Boosting peroxisome numbers with PEX11B inhibits Zika virus replication and enhances interferon signaling.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Zika virus (ZIKV) causes congenital defects and neurological issues.
- The interferon (IFN) system is key to controlling ZIKV.
- Peroxisomes are emerging as critical signaling platforms for antiviral responses.
Purpose of the Study:
- To investigate ZIKV's impact on peroxisome biogenesis.
- To understand peroxisomes' role in ZIKV antiviral signaling and neuropathogenesis.
Main Methods:
- Studied ZIKV infection in human fetal astrocytes.
- Assessed peroxisome numbers and PEX11B expression.
- Analyzed IFN-dependent antiviral signaling pathways.
Main Results:
- ZIKV infection significantly depletes peroxisomes in astrocytes.
- The peroxisome biogenesis factor PEX11B inhibits ZIKV replication.
- PEX11B enhances IFN-dependent antiviral signaling.
Conclusions:
- Peroxisome depletion by ZIKV compromises antiviral defenses in brain cells.
- PEX11B-mediated enhancement of peroxisomes offers a potential therapeutic strategy against ZIKV.
- Peroxisomes are crucial regulators of ZIKV neuropathogenesis.
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