Microglia in Memory Decline from Zika Virus and West Nile Virus Infection

Jennifer Tisoncik-Go1, Michael Gale2

  • 1Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA, USA; Department of Immunology, University of Washington, Seattle, WA, USA; Washington National Primate Research Center, Seattle, WA, USA.

Trends in Neurosciences
|September 10, 2019
PubMed

Insights

Persistent T cells in the brain after neurotropic viral infections, like Zika virus (ZIKV) and West Nile virus (WNV), can cause cognitive decline. This is due to T cell-produced interferon-gamma activating microglia.

Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • Neurotropic viral infections can lead to long-term neurological issues.
  • Persistent T cell infiltration in the brain is associated with cognitive impairment following viral encephalitis.

Purpose of the Study:

  • To investigate the role of T cell-derived interferon-gamma (IFN-γ) in cognitive decline post-Zika virus (ZIKV) and West Nile virus (WNV) infection.
  • To elucidate the mechanism by which T cells contribute to neuroinflammation and cognitive deficits during viral recovery.

Main Methods:

  • The study analyzed immune responses in the brain following ZIKV and WNV infections.
  • Investigated the impact of T cell-produced IFN-γ on microglial activation and cognitive function.

Main Results:

  • Sustained T cell presence in the brain was observed during the recovery phase.
  • T cell production of IFN-γ was found to directly mediate microglia activation.
  • This IFN-γ-induced microglia activation correlated with observed cognitive decline.

Conclusions:

  • Interferon-gamma produced by persistent T cells is a key driver of cognitive decline after ZIKV and WNV infections.
  • Targeting T cell-mediated IFN-γ signaling could be a therapeutic strategy for post-viral cognitive impairment.

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