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‘Accidental’ Breakthrough Helps Develop New Ways to Prevent Flu
Researchers found H1N1 and H3N2 use different routes into lung cells, revealing a strain-specific target that could help block flu replication.
Researchers at the University in Vermont led by Emily Bruce discovered that H1N1 and H3N2 influenza viruses enter lung cells using different strategies, challenging the assumption that all flu viruses infect cells identically.
Scientists previously believed all influenza viruses utilized the same entry mechanism; researchers 'accidentally' discovered that distinct viruses use unique strategies to infiltrate cells, which Bruce likened to pirates hijacking ships.
Data revealed that H3N2 viruses require a specific protein, Rab11B, to enter human lung cells; when the team depleted Rab11B, H3N2 viruses failed to enter, unlike H1N1.
American researchers say the discovery provides "fundamental insights" into how viruses infect people, highlighting a path for developing better medications; Bruce emphasized a "dire" need for treatments to stop viral replication.
Scientists aim to use this discovery to prevent distinct flu viruses from entering cells, with future studies investigating whether Rab11B-dependency is a fundamental property of H3N2 or unique to currently circulating strains.