ReviewVirus genes2026
Divergent mechanistic reliance on the phosphatidylinositol 4-kinase (PI4K)/oxysterol-binding protein (OSBP) axis during Zika virus versus dengue virus and West Nile virus replication organelle biogenesis.
Review in Virus genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Positive-strand RNA viruses remodel host endoplasmic reticulum (ER) membranes into replication organelles (ROs) that support genome replication. Members of the genus Orthoflavivirus exploit host lipid pathways, particularly the phosphatidylinositol 4-kinase (PI4K)-phosphatidylinositol 4-phosphate (PI4P)-oxysterol-binding protein (OSBP) axis, yet they display marked mechanistic divergence. Specifically, it raised a central and unresolved question: is local PI4P enrichment an indispensable determining factor for viral vesicle biogenesis, or is it merely a contributing factor to a more fundamental, underlying mechanical requirement for high membrane curvature? Zika virus (ZIKV) shows strong dependence on PI4P enrichment. ZIKV nonstructural protein 1 (NS1) binds negatively charged lipids, including PI4P, via a positively charged membrane-binding surface that includes Arg31. This interaction supports NS1-mediated ER remodeling and subsequent OSBP-mediated cholesterol delivery. In contrast, dengue virus (DENV) and West Nile virus (WNV) largely bypass strict PI4P dependence. Their RO biogenesis relies more heavily on viral membrane proteins (NS4A/NS4B), host reticulon RTN3.1A, alternative lipid-shape remodeling (including phospholipase A2-generated lysophosphatidylcholine in WNV, sterol availability, and fatty-acid synthesis. Beyond the PI4P-OSBP axis, virus-specific exploitation of lipid peroxidation (ALOX12 pathway), cholesteryl-ester-enriched lipid droplets (via SOAT1/SOAT2), nuclear lipid droplets, and glycerophospholipid/ceramide remodeling further differentiates these viruses. These distinctions have direct implications for host-targeted antivirals. PI4K and OSBP inhibitors show preferential activity against ZIKV, whereas SOAT1/2 inhibition exhibits broader anti-orthoflaviviral potential, and other targets (FASN, NAAA, ALOX12) display virus-weighted efficacy. Recognition of this mechanistic spectrum is essential for accurate interpretation of lipid-perturbation studies and for the rational design of broad-spectrum or virus-selective antiviral strategies.
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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 Socratic graph.