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FPR2: A Novel Promising Target for the Treatment of Influenza
Marie-Christine Alessi1, Nicolas Cenac2, Mustapha Si-Tahar3
1Aix Marseille Univ, INSERM, INRA, NORT, UMR 1260/1062Marseille, France.
Abstract:
The Formyl-peptide receptor-2 (FPR2) is a seven transmembrane G protein-coupled receptor, which plays an important role in sensing of bacteria and modulation of immune responses. FPR2 is also used by viruses for their own profit. Annexin A1, one of the multiple ligands of FPR2, is incorporated in the budding virus membrane of influenza A viruses (IAV). Thereby, once IAV infect a host cell, FPR2 is activated. FPR2-signaling leads to an increase in viral replication, a dysregulation of the host immune response and a severe disease. Conversely, experiments using FPR2 antagonists in a preclinical model of IAV infections in mice showed that blocking FPR2 protects animals from lethal infections. Thus, FPR2 represents a very attractive host target against influenza. In this review we will give an overview on the pathogenesis of influenza with a focus on the role of FPR2 and we will discuss the advantages of using FPR2 antagonists to treat the flu.
Insights
Formyl-peptide receptor-2 (FPR2) aids influenza A virus (IAV) replication and disease. Blocking FPR2 with antagonists protects against lethal flu infections, offering a potential therapeutic strategy.
Area of Science:
- Immunology
- Virology
- Pharmacology
Background:
- Formyl-peptide receptor-2 (FPR2) is a G protein-coupled receptor involved in immune responses.
- Viruses, including influenza A virus (IAV), exploit FPR2 for replication.
- Annexin A1, an FPR2 ligand, is incorporated into IAV, activating FPR2 upon infection.
Purpose of the Study:
- To review the role of FPR2 in influenza pathogenesis.
- To discuss FPR2 antagonists as a potential therapeutic strategy against influenza.
Main Methods:
- Literature review focusing on FPR2's role in influenza A virus infection.
- Analysis of preclinical data on FPR2 antagonist efficacy in mouse models.
Main Results:
- FPR2 activation by IAV-associated Annexin A1 enhances viral replication.
- FPR2 signaling dysregulates host immune responses, leading to severe disease.
- FPR2 antagonists demonstrated protective effects against lethal IAV infection in mice.
Conclusions:
- FPR2 is a critical host factor exploited by IAV.
- Targeting FPR2 with antagonists presents a promising therapeutic avenue for treating influenza.
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