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Dual NDP52 Function in Persistent CSFV Infection.

Shuangqi Fan1, Keke Wu1, Chaowei Luo1

  • 1College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.

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|January 24, 2020
PubMed
Summary
This summary is machine-generated.

Classical swine fever virus (CSFV) evades immune responses by inhibiting the autophagy receptor NDP52. Inhibiting NDP52 blocks CSFV entry into autophagosomes and activates antiviral pathways, offering new therapeutic strategies.

Keywords:
CD63NDP52NF-κBclassical swine fever virusubiquitination

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Viruses employ diverse strategies to circumvent host antiviral defenses.
  • Classical swine fever virus (CSFV) utilizes autophagy for replication and immune evasion.
  • Mechanisms of CSFV autophagosome entry and autophagy-mediated replication are poorly understood.

Purpose of the Study:

  • To elucidate the role of the autophagy receptor NDP52 in CSFV infection.
  • To investigate how CSFV manipulates autophagy and host antiviral responses.
  • To identify novel therapeutic targets for CSFV.

Main Methods:

  • Investigated the effect of CSFV infection on NDP52 expression, ubiquitination, and SUMOylation.
  • Utilized Pten-induced kinase 1 (PINK1)-Parkin pathway analysis.
  • Assessed the impact of NDP52 inhibition on CSFV replication, CD63 expression, and NF-κB pathway activation.

Main Results:

  • CSFV infection inhibits NDP52 expression and modification via the PINK1-Parkin pathway.
  • NDP52 inhibition reduces CSFV binding to autophagic vesicles and viral replication.
  • Inhibition of NDP52 enhances interferon and TNF release, activating the NF-κB antiviral pathway.

Conclusions:

  • NDP52 plays a critical role in CSFV infection by facilitating viral entry into autophagosomes and suppressing innate immunity.
  • CSFV subverts autophagy through NDP52 manipulation to promote persistent infection.
  • Targeting NDP52 presents a promising strategy for developing novel antiviral therapies against CSFV.