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Updated: Dec 14, 2025
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Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
Published on: August 23, 2016
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A global lipid map defines a network essential for Zika virus replication
Hans C Leier1, Jules B Weinstein1, Jennifer E Kyle2
1Department of Molecular Microbiology & Immunology, Oregon Health & Science University (OHSU), Portland, OR, 97239, USA.
Nature Communications
|July 23, 2020
Summary
Zika virus (ZIKV) infection alters host sphingolipid metabolism. This study reveals ceramide accumulation at replication sites, highlighting sphingolipids as key targets for ZIKV.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Zika virus (ZIKV) is a global health concern that remodels host cell membranes for replication.
- The precise mechanisms by which ZIKV disrupts lipid networks and the consequences for disease pathogenesis remain unclear.
Purpose of the Study:
- To investigate the role of host lipid metabolism, specifically sphingolipids, in ZIKV replication.
- To map the lipid network alterations induced by ZIKV infection.
Main Methods:
- Comprehensive lipidomics was employed to analyze lipid composition during ZIKV infection.
- The function of ZIKV NS4B protein in lipid modulation was assessed.
- Sphingolipid biosynthesis was disrupted in various cell types, including human neural progenitor cells.
Main Results:
- ZIKV infection significantly altered host lipid profiles, with notable changes in sphingolipid subclasses.
- ZIKV NS4B protein expression mimicked these sphingolipid alterations, implicating it in pathway modulation.
- Disrupting sphingolipid biosynthesis inhibited ZIKV replication.
- The sphingolipid ceramide localized to ZIKV replication sites, and elevated ceramide levels increased cellular susceptibility to ZIKV.
Conclusions:
- A sphingolipid metabolic network critical for ZIKV replication was identified.
- Ceramide flux was established as a key mediator of ZIKV infection, suggesting potential therapeutic targets.
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