Picornavirus VP3 protein induces autophagy through the TP53-BAD-BAX axis to promote viral replication

Ruoqing Mao1, Zixiang Zhu1, Fan Yang1

  • 1State Key Laboratory for Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.

Autophagy
|May 16, 2024
PubMed

Insights

Picornaviruses hijack host cell autophagy via the VP3 protein, utilizing the TP53-BAD-BAX pathway to enhance viral replication and pathogenesis. Targeting this interaction offers a strategy for broad-spectrum antiviral development.

Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Macroautophagy/autophagy and apoptosis are critical host responses to viral infections, including those caused by picornaviruses.
  • Picornaviruses are known to manipulate host cell processes, but the specific mechanisms involving autophagy and apoptosis require further elucidation.

Purpose of the Study:

  • To investigate the role of picornavirus VP3 proteins in triggering autophagy and apoptosis.
  • To elucidate the mechanism by which picornaviruses, using foot-and-mouth disease virus (FMDV) as a model, hijack autophagy for replication and pathogenesis.
  • To identify key viral components and host factors involved in this process for potential therapeutic targeting.

Main Methods:

  • Utilized FMDV as a model system to study viral-induced autophagy and apoptosis.
  • Investigated the interaction between FMDV VP3 protein and host factors, including TP53, BAD, and BAX.
  • Employed genetic mutations (Gly129 to Ala129 in VP3) to assess the functional importance of specific viral amino acids.
  • Assessed viral replication and pathogenesis in vitro and in vivo.

Main Results:

  • FMDV VP3 protein induces both autophagy and apoptosis by facilitating TP53 translocation to mitochondria, activating the BAD-mediated apoptosis and BECN1-mediated autophagy pathways.
  • Amino acid Gly129 in VP3 is essential for TP53 interaction, autophagy, and apoptosis induction, crucial for FMDV replication and pathogenesis.
  • Mutation of Gly129 abrogated VP3's autophagic function, significantly reducing viral replication and pathogenesis, indicating VP3-induced autophagy benefits the virus.

Conclusions:

  • Picornavirus VP3 protein hijacks host autophagy through the TP53-BAD-BAX axis, essential for viral replication and pathogenesis.
  • The conserved Gly129 residue in VP3 plays a critical role in mediating these viral-host interactions.
  • This mechanism provides a potential target for developing broad-spectrum antivirals and attenuated vaccines against picornaviruses.

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