New experimental data pinpoints a molecular component responsible for modulating the damage the flu can wreck on the lungs. The molecule, known as DAF, increases disease severity in mice upon infection with Influenza A virus, the most prevalent cause of the seasonal flu. Understanding this novel virulence mechanism of influenza and identifying the intrinsic factors that determine disease severity opens new possibilities for finding therapeutic targets for resilience to viral infections.
The seasonal flu kills up to 600 000 people a year worldwide and has a century-long history of pandemics. Examples include the Spanish flu in the late 1910’s or the H1N1 in 2009, which together claimed more than 50 million lives. “The way the stage is set tells us that it is not a matter of if but rather of when there will be a next pandemic. And preparing ourselves for that demands intensive fundamental research and constant accumulation of knowledge about these viruses and the diseases they cause”, says Maria João Amorim, IGC principal investigator and leader of the team that conducted the study.
When a virus like influenza enters our lungs, it is quickly faced with cocktails of molecules that recognize it and alert the host of its presence. Signals flow back and activate the immune response, calling in an army of cells and inflammation sidekicks. Any exaggeration can destabilize the equilibrium needed to clear the virus and spare our tissues from damage. For most people, clearance arrives a few days after infection and leaves very few traces. But for some, influenza infection entails severe complications, resulting from an exacerbated response that damages the lungs.
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