An unexpected laboratory finding has revealed a completely new way to stop influenza viruses from spreading, according to researchers from the University of Vermont’s Larner College of Medicine.

While studying how influenza replicates inside human cells, scientists found that different strains use entirely different methods to gain entry, as first reported by SWNS.

By identifying and targeting the exact molecules these viruses rely on, the team discovered they could prevent viral entry and halt replication altogether.

Lead investigator Dr. Emily Bruce described the discovery as a major step toward developing improved preventive treatments for influenza infections.

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“The hope is that fundamental, curiosity-based research like this helps to pave the way for novel strategies to treat and prevent influenza infections,” Bruce said in the SWNS report.

The study, published in The Journal of Virology, began as an effort to map how viral RNA moves within infected cells during the process of forming new viral particles.

Researchers tested both H1N1 and H3N2 influenza A viruses using isolates obtained from patient nasal samples collected in 2022.

During the experiments, the team unexpectedly uncovered a previously unknown pathway that blocked the virus from entering lung cells.

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When the scientists depleted a specific human protein known as Rab11B, H3N2 viruses were unable to invade lung cells, whereas H1N1 continued unaffected.

Using reverse genetics, they traced this defect and identified a newly defined, strain-specific role for Rab11B in allowing H3N2 entry into cells.

The finding overturned a long-held scientific belief that all flu viruses enter human cells by the same route.

“Viruses are like pirates from different countries hijacking someone’s ship,” Bruce explained. “Different viruses, like different types of pirates, use different methods to get onboard.”

She added that while researchers previously assumed all strains used the same mechanism, the data proved that H1N1 and H3N2 depend on different cellular proteins to infect new cells.

According to Bruce, eliminating the correct protein could effectively block a specific virus from spreading further in the body.

Despite the promising insight, the study’s experiments were performed on isolated cells in the laboratory.

The research team cautioned that more work is required to confirm whether this mechanism operates safely and effectively within living respiratory systems.

They also plan to investigate whether the Rab11B-dependent process is a permanent characteristic of H3N2 viruses or a feature of those now circulating.

These findings could eventually help design new preventive drugs that target specific viral entry points, potentially reducing the spread of influenza in the future.

Former U.S. Surgeon General Dr. Jerome Adams noted that the new variant spreading across the country has already led to record hospitalizations, underscoring the need for breakthroughs like this one.

The new research highlights how unexpected laboratory results can lead to fundamental discoveries that reshape how scientists approach long-standing public health challenges.