ArticleNature communications2020
A global lipid map defines a network essential for Zika virus replication.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
66 citing papers in PubMed, 94 citations in OpenAlex.
- Review
- Reciprocal control of viral infection and phosphoinositide dynamics.FEBS letters · 2026Review
- Reprogramming lipid metabolism in virus-infected neuronal cells.Research square · 2026Article
- The K247 ubiquitination site of the Newcastle disease virus M protein enhances viral budding to facilitate rapid exploitation of host cell sphingolipid metabolites.Poultry science · 2026Article
- Lipid Architecture in the Zika Virus.ACS physical chemistry Au · 2026Article
- iPLA2β-dependent phospholipid remodeling drives ZIKV-induced neuroinflammation and neurological injury.Journal of neuroinflammation · 2026Article
- Integrative proteomics and lipidomics reveals dual roles for lipid droplets in the host cell antiviral response.Nature communications · 2026Article
- Behind the membranous curtain-lipid dynamics and functions in coronaviral replication.Journal of virology · 2026Review
- Emerging roles of lipids in the flavivirus life cycle.Trends in microbiology · 2026Review
- Mammarenaviruses depend on endogenous fatty acid synthesis in cell culture systems.Journal of lipid research · 2026Article
- A non-canonical JAK/STAT pathway promotes viral replication through the lipoprotein receptor-related protein in ticks.PLoS biology · 2026Article
- Spatially and temporally comparative proteomics provide insights into dynamic response patterns to PEDV infection.Communications biology · 2026Article
- Fatty acid transporter protein isoform 2 (FATP2) inhibitor lipofermata inhibits Zika virus replication and blocks fatty acid uptake in SH-SY5Y neuroblastoma cell line.Microbiology spectrum · 2026Article
- Downmodulation of cholesterol biosynthetic network governs activation of the innate immune response to Japanese encephalitis virus infection.Journal of virology · 2026Article
- Lipidomics reveals the pro-viral roles of ceramides during fish nodavirus infection.Journal of virology · 2026Article
- Article
- Measles virus reprograms CD4Frontiers in cell and developmental biology · 2026Article
- Dynamic regulatory mechanism of cholesterol 25-hydroxylase-mediated antiviral response in RNA virus infections.Frontiers in cellular and infection microbiology · 2026Review
- The inhibition mechanism ofFrontiers in microbiology · 2026Review
- Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Zika virus (ZIKV), an arbovirus of global concern, remodels intracellular membranes to form replication sites. How ZIKV dysregulates lipid networks to allow this, and consequences for disease, is poorly understood. Here, we perform comprehensive lipidomics to create a lipid network map during ZIKV infection. We find that ZIKV significantly alters host lipid composition, with the most striking changes seen within subclasses of sphingolipids. Ectopic expression of ZIKV NS4B protein results in similar changes, demonstrating a role for NS4B in modulating sphingolipid pathways. Disruption of sphingolipid biosynthesis in various cell types, including human neural progenitor cells, blocks ZIKV infection. Additionally, the sphingolipid ceramide redistributes to ZIKV replication sites, and increasing ceramide levels by multiple pathways sensitizes cells to ZIKV infection. Thus, we identify a sphingolipid metabolic network with a critical role in ZIKV replication and show that ceramide flux is a key mediator of ZIKV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.