An accidental lab discovery is changing how scientists understand influenza, revealing that different strains use completely different strategies to enter human cells.
Researchers at the University of Vermont's Larner College of Medicine found that targeting specific molecules can block flu viruses from entering new cells and halt replication. The study, published in The Journal of Virology, originally aimed to map viral RNA transport but unexpectedly uncovered a cellular pathway that stopped the virus from infecting lung cells.
The key discovery: when a human protein called Rab11B is depleted, H3N2 viruses fail to enter lung cells, while H1N1 viruses remain unaffected. This challenges the long-held assumption that all flu viruses enter cells the same way.
"We had previously thought that all flu viruses used the same way to get into a cell, but we discovered that this is not true," said principal investigator Dr. Emily Bruce. "H1N1 and H3N2 need different proteins to get in, and if you get rid of the right protein, a specific virus can’t get in."
The study used H1N1 and H3N2 viruses isolated from patients in 2022. Researchers caution that further testing is needed to determine if blocking the protein is safe in a live respiratory system. Bruce hopes to explore whether this Rab11B dependency is a fundamental property of H3N2 or unique to current circulating strains.