Influenza (flu) can be fatal, but just how it causes severe damage to the lungs has been a mystery….until now.
New research has identified a protein which acts as a "self-destruct button" in the lungs, opening the door to new treatments that fight the disease.
Influenza causes up to 650,000 deaths globally each year and severe flu can lead to hospitalisation, lung failure, and long-term health issues, but that's not the worst of it, according to Associate Professor Michelle Tate.
She specialises in understanding how hyperinflammation develops in severe respiratory disease, and she warns that current treatment options are limited, and resistance to antiviral drugs is rising.
Reducing lung damage from flu
"Every year, thousands of people, especially adults 65+ and those with weakened immune system, get seriously ill from the flu," A/Prof Tate said. "Our findings could lead to new medicines that reduce lung damage and inflammation, helping people recover faster and lowering the risk of death from severe flu."
So, what are these findings, and why are they important?
Working with PhD Student, Sarah Rosli, A/Prof Tate uncovered a new way the body responds to the influenza virus.
"We found that a protein called Gasdermin E plays a major role in causing lung damage during influenza. By deleting this protein, we were able to reduce inflammation and improve survival," she said.
"We discovered that Gasdermin E acts like a 'self-destruct' button in lung epithelial cells during infection, causing them to burst and release inflammatory signals."
She said the actions of this protein lead to more tissue damage and worsen illness.
A pathway to less severe flu
"When we removed this protein, the lungs stayed healthier, and the flu was less severe. This opens up exciting possibilities for new treatments that help the body fight flu more effectively."
This world-first study shows that a protein Gasdermin E is activated by multiple strains of the influenza virus and plays a central role in triggering epithelial cell death and uncontrolled inflammation.
"By blocking this pathway, we were able to reduce inflammation and viral replication, pointing to a new way to treat severe flu across different virus types," Ms Rosli said.
This research is published in Cell Death & Disease.
