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PI3Kγ Pathway Contributes to Neuroinflammation and Neuronal Death Induced by Zika Virus Infection.

Danielle Cunha Teixeira1, Gabriel Campolina-Silva2,3, Fernanda Martins Marim4

  • 1Department of Morphology, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.

Immunology
|February 7, 2026
PubMed
Summary

The PI3Kγ pathway fuels Zika virus replication and neuroinflammation. Inhibiting PI3Kγ protects neurons, reduces viral load, and lessens brain damage in ZIKV infection models.

Keywords:
NeuroinflammationPI3K/AKT pathwayZika virus (ZIKV)microglia activationneuronal cell deathphosphatidylinositol 3‐kinase γ (PI3Kγ)

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Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • Zika virus (ZIKV) targets the central nervous system (CNS), causing neuroinflammation and neuronal death.
  • ZIKV utilizes host cell pathways, like PI3K/AKT, for replication and apoptosis evasion.
  • The specific role of the PI3Kγ isoform in ZIKV pathogenesis remained unexplored.

Purpose of the Study:

  • To investigate the role of PI3Kγ signaling in ZIKV pathogenesis.
  • To assess the impact of PI3Kγ inhibition on viral replication and neuronal survival.
  • To evaluate PI3Kγ's role in ZIKV-induced neuroinflammation in vivo.

Main Methods:

  • Primary neuronal cultures and human neuroblastoma cells were infected with ZIKV after PI3Kγ genetic ablation or pharmacological inhibition.
  • Interferon α/β receptor knockout (A129) mice were treated with a PI3Kγ inhibitor (AS605240) before or after ZIKV infection.
  • Viral load, neuronal death, microglial TNF production, CD8+ T cell activation, and pro-inflammatory cytokine levels were assessed.

Main Results:

  • PI3Kγ inhibition (genetic or pharmacological) suppressed ZIKV replication and prevented neuronal death in vitro.
  • In vivo, PI3Kγ inhibition reduced viral load, brain/optic nerve damage, and microglial TNF production.
  • Inhibition decreased CD8+ T cell recruitment/activation and pro-inflammatory mediators (IFN-γ, IL-17) in ZIKV-infected mouse brains.

Conclusions:

  • PI3Kγ activation promotes ZIKV infection and exacerbates neuroinflammation.
  • Pharmacological inhibition of PI3Kγ offers neuroprotection against ZIKV.
  • Targeting PI3Kγ may be a therapeutic strategy for ZIKV infections.