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Peli1 facilitates virus replication and promotes neuroinflammation during West Nile virus infection

Huanle Luo1, Evandro R Winkelmann1, Shuang Zhu2

  • 1Department of Microbiology and Immunology.

The Journal of Clinical Investigation
|September 25, 2018
PubMed

Insights

Pellino 1 (Peli1) deficiency protects against lethal West Nile virus (WNV) by reducing viral load and brain inflammation. Peli1 is unexpectedly crucial for WNV entry and replication in various cells.

Area of Science:

  • Neuroimmunology
  • Virology
  • Cell Biology

Background:

  • Pellino 1 (Peli1), an E3 ubiquitin ligase, is a microglia-specific mediator of autoimmune encephalomyelitis.
  • The function of Peli1 in neurotropic flavivirus infections remains largely unknown.

Purpose of the Study:

  • To investigate the role of Peli1 in West Nile virus (WNV) infection.
  • To determine Peli1's involvement in viral entry, replication, and host immune response.

Main Methods:

  • Utilized Peli1-deficient (Peli1-/-) and wild-type (WT) mice models.
  • Assessed viral loads, brain inflammation, and immune cell infiltration.
  • Examined WNV entry and replication in macrophages, neurons, and microglia.
  • Analyzed patient postmortem tissues.

Main Results:

  • Peli1-/- mice showed increased resistance to lethal WNV infection, with reduced viral loads and brain inflammation.
  • Peli1 deficiency attenuated T cell and macrophage infiltration into the central nervous system (CNS).
  • Peli1 was essential for WNV entry and replication in mouse and human cells, and highly expressed in infected patient tissues.

Conclusions:

  • Peli1 plays a non-immune regulatory role in promoting microglia activation during WNV infection.
  • Peli1 is a potential host factor facilitating flavivirus cell entry and replication.
  • Targeting Peli1 could offer a novel therapeutic strategy against WNV and potentially other flaviviruses.
Keywords:
InflammationInnate immunityNeurological disordersVirology

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