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Related Experiment Video

Updated: May 14, 2026

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

Zika Virus-Induced Metabolic Reprogramming Drives Lipid Droplet Biogenesis, Promoting Viral Replication and Ocular

Prince Kumar1, Jieon Kim1, Nikhil Deshmukh1

  • 1Department of Ophthalmology, Mason Eye Institute, University of Missouri School of Medicine, 1 Hospital Dr, Columbia, MO 65212, USA.

Cells
|May 13, 2026
PubMed
Summary

Zika virus (ZIKV) alters cell metabolism in the eye's trabecular meshwork (TM). Targeting AMP-activated protein kinase (AMPK) and lipid metabolism shows potential for treating ZIKV-related eye diseases.

Keywords:
AMPKZika virusenergy metabolismfatty acidsglaucomalipid dropletlipid metabolismtrabecular meshworkβ-oxidation

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Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids

Published on: September 19, 2017

Area of Science:

  • Ophthalmology
  • Virology
  • Cellular Metabolism

Background:

  • Zika virus (ZIKV) causes severe neurological and ocular issues, including congenital glaucoma.
  • Viruses hijack host metabolism for replication, but ZIKV's impact on ocular metabolic pathways is unclear.
  • Trabecular meshwork (TM) cells are crucial for aqueous humor outflow and eye pressure regulation.

Purpose of the Study:

  • To investigate how ZIKV infection reprograms energy and lipid metabolism in human TM cells.
  • To explore the roles of AMP-activated protein kinase (AMPK) signaling, fatty acid (FA) metabolism, and lipid droplet (LD) biogenesis in ZIKV ocular pathogenesis.
  • To assess potential therapeutic targets within these metabolic pathways for ZIKV-associated eye complications.

Main Methods:

  • Primary human TM cells and an IFNAR1-deficient mouse model were used.
  • ZIKV infection effects on AMPK signaling, FA metabolism, and LD accumulation were analyzed.
  • Pharmacological modulators of AMPK, DGAT1, and FA metabolism were applied to assess viral replication.

Main Results:

  • ZIKV infection activated the LKB1-AMPK-ACC pathway, with AMPK activation showing antiviral effects.
  • ZIKV promoted lipid droplet (LD) biogenesis, and DGAT1 inhibition reduced LDs and viral replication, indicating a proviral role for LDs.
  • Saturated fatty acids (palmitate) enhanced ZIKV replication, while unsaturated fatty acids (oleate, linoleate) inhibited it by affecting viral entry.

Conclusions:

  • ZIKV manipulates AMPK signaling, FA metabolism, and LD biogenesis in TM cells to facilitate its replication and spread within ocular tissues.
  • Differential modulation of these metabolic pathways offers potential therapeutic strategies for ZIKV-induced ocular diseases.
  • Targeting host metabolic reprogramming presents a promising avenue for managing ZIKV-related ophthalmic complications.