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G protein-coupled receptor 17 restricts rabies virus replication via BAK-mediated apoptosis.

Abstract
Rabies, caused by rabies virus (RABV), is an ancient zoonotic disease that significantly affects human and animal health throughout the world. RABV causes acute encephalitis in mammals with a high fatality rate in developing countries. G protein-coupled receptor 17 (GPR17) is a vital gene in the central nervous system (CNS) that plays important roles in demyelinating diseases and ischemia brain. However, it is still unclear whether GPR17 participates in the regulation of RABV infection. Here, we found that upregulation or activation of GPR17 can reduce the virus titer; conversely, the inactivation or silence of GPR17 led to increased RABV replication in N2a cells. The recombinant RABV expressing GPR17 (rRABV-GPR17) showed reduced replication capacity compared to the parent virus rRABV. Moreover, overexpression of GPR17 can attenuate RABV pathogenicity in mice. Further study demonstrated that GPR17 suppressed RABV replication via BAK-mediated apoptosis. Our findings uncover an unappreciated role of GPR17 in suppressing RABV infection, where GPR17 mediates cell apoptosis to limit RABV replication and may be an attractive candidate for new therapeutic interventions in the treatment of rabies.
AuthorsWei Liu, Yaping Yang, Zonghui Zeng, Yuling Tian, Qiong Wu, Ming Zhou, Zhen F Fu, Ling Zhao
JournalVeterinary microbiology (Vet Microbiol) Vol. 265 Pg. 109326 (Feb 2022) ISSN: 1873-2542 [Electronic] Netherlands
PMID34979406 (Publication Type: Journal Article)
CopyrightCopyright © 2021 Elsevier B.V. All rights reserved.
Chemical References
  • Bak1 protein, mouse
  • GPR17 protein, mouse
  • Nerve Tissue Proteins
  • Receptors, G-Protein-Coupled
  • bcl-2 Homologous Antagonist-Killer Protein
Topics
  • Animals
  • Apoptosis
  • Mammals
  • Mice
  • Nerve Tissue Proteins (metabolism)
  • Rabies (metabolism, virology)
  • Rabies virus (physiology)
  • Receptors, G-Protein-Coupled (metabolism)
  • Virus Replication
  • bcl-2 Homologous Antagonist-Killer Protein (metabolism)

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