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An accidental lab discovery has opened the door to entirely new ways of preventing the flu.
While investigating how influenza replicates, researchers discovered that different flu strains use completely different strategies to infiltrate human cells, SWNS reported.
By targeting the specific molecules the viruses rely on, scientists found that they could block them from entering new cells and halt their replication altogether.
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Researchers say these “fundamental insights” into seasonal influenza highlight a clear path toward developing better preventive medications.
“The hope is that fundamental, curiosity-based research like this helps to pave the way for novel strategies to treat and prevent influenza infections,” principal investigator Dr. Emily Bruce, from the University of Vermont’s Larner College of Medicine, said in the SWNS report.
While investigating how influenza replicates, researchers discovered that different flu strains use completely different strategies to infiltrate human cells. (iStock)
While several flu strains cause illness, H1N1 and H3N2 influenza A viruses are the most common. However, current flu tests cannot differentiate between them, and clinical treatments are identical for both.
Although vaccines and antivirals are available, Bruce noted a “dire” need for better medications to stop the virus from spreading cell to xxcell.
“You don’t get sick when a virus is in one cell,” he noted. “You get sick because a virus replicates itself and goes into many more cells.”
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The study, which was published in The Journal of Virology, originally aimed to map how viral RNA segments are transported within cells to create new viral particles.
The team used H1N1 and H3N2 viruses isolated from the nasal passages of positive patients in 2022.
Clinical treatments remain identical for both primary strains of the flu virus. (iStock)
During the investigation, the team unexpectedly stumbled upon a cellular pathway that blocked the virus from entering lung cells, SWNS reported.
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The data revealed that when a specific human protein called Rab11B was depleted, H3N2 viruses failed to enter human lung cells. H1N1 viruses were completely unaffected.
Using reverse genetics, the team mapped this defect and uncovered a brand-new, H3N2-specific role for Rab11B during viral entry.
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This discovery challenged the scientific assumption that all flu viruses enter cells the same way.
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“Viruses are like pirates from different countries hijacking someone’s ship,” Bruce said. “Different viruses, like different types of pirates, use different methods to get onboard.”
This discovery challenged the scientific assumption that all flu viruses enter cells the same way. (iStock)
“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,” she went on. “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.”
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While these findings identify a critical cellular pathway for viral entry, the study was conducted using isolated cells, the researchers acknowledged.
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Further research is needed to determine whether blocking the protein is safe and effective within a live, complex human respiratory system.
Bruce and the team hope to conduct further research to determine whether this Rab11B-dependency is a fundamental property of H3N2, or if it’s a trait unique to currently circulating flu strains.