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.
Highlights
Influenza virus infection is one of the most important infectious diseases affecting the respiratory tract (Palese and Shaw, 2007)
Since all Formyl peptide receptors (FPR) have a high degree of sequence homology, these results are consistent with the protective effect of FPR2 antagonists against flu and suggest that other FPR might be involved in influenza A viruses (IAV) pathogenesis
Preclinical studies have proven that FPR2 antagonists efficiently protect mice against IAV infections, by inhibiting viral replication and deleterious inflammation of the lungs
Summary
Influenza virus infection is one of the most important infectious diseases affecting the respiratory tract (Palese and Shaw, 2007). The etiological agents of the disease are the negative sense and single-stranded RNA influenza viruses, which belong to the family of enveloped viruses. The host immune response is activated in order to limit viral replication and to eliminate infected cells. The main specific sensors activated by influenza viruses are TLR3/7/8, NLRP3 and RIG-I. The secretion of pro-inflammatory cytokines and chemokines attracts and activates innate immune cells such as natural killer cells, neutrophils and macrophages, that can afford an effective protection by eliminating influenza virusinfected cells (Kuiken et al, 2012). The main factors contributing to a severe disease are the high capacity of influenza virus to replicate and a dysregulated harmful innate immune response
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