BACKGROUND
Despite vaccination, 5 million people are affected each year by the influenza virus in the world, causing more than 500,000 deaths annually.
Current antivirals (neuraminidase, hemagglutinin and M2 protein inhibitors) are no longer effective 48 hours after infection and lead to the emergence of multi-drug resistance strains. Need for new antivirals with broad spectrum activity remains high to prevent epidemics and pandemics.
HOW IT WORKS
FPR2 (Formyl Peptide Receptor 2) plays a key role through the ERK / MAPK pathway in the inflammatory resolution following an acute inflammation but also in the replicative capacity of the influenza virus.
Researchers show that an antagonist of FPR2 protects mice against influenza infection by blocking viral replication, as well as significantly reducing pulmonary inflammation.
KEY BENEFITS
•FPR2 is a new target involved in influenza infection
•FPR2 inhibition permits new therapeutic strategy to fight influenza by targeting a host protein instead of viral proteins, limiting the emergence of viral resistance:
-may be effective against all flu virus strain
-effective much longer after the first 48 hours after infection
•FPR2 isn't a main physiological pathway, unlike NF-kB and ERK: side effects will be much less important than the strategies targeting NF-kB or ERK
DEVELOPMENT STATUS
•In vitro and in vivo in mice results on H1N1 and H3N2 influenza strains
•In progress:
-test of other FPR2 antagonists
-preventive effect (pretreatment)
-efficacy on other strains (B type)
APPLICATIONS
Treatment of seasonal and pandemic influenza (human and animal)