How Do Flu Strains Evolve to Become Airborne?

Not all flu virus strains are created equal. After all, some are better equipped to transmit from host to host than others and new research has pinpointed an intricate factor that allows the virus to do so through the air.

Not all flu virus strains are created equal. After all, some are better equipped to transmit from host to host than others and new research has pinpointed an intricate factor that allows the virus to do so through the air.

Flu viruses come in different strains — with influenza A (H1N1), influenza A (H3N2), and influenza B viruses being the most common during the 2014-2015 season. While analyzing the H1N1 strain, researchers from the Massachusetts Institute of Technology (MIT) discovered that the soft palate plays an important role in airborne transmissibility.

Previous research by one of the senior authors, Ram Sasisekharan, concluded that a virus’ airborne transmissibility was reliant on if its hemagglutinin (HA) protein could bind to receptors found on the surface of human respiratory cells. While some flu viruses better attach to the alpha 2-6 glycan receptors that are mostly found in humans and other mammals, different strains better bind to alpha 2-3 glycan receptors that are more commonly observed in birds. The new study published in Nature takes the investigation a step further.

The H1N1 strain, which killed more than 250,000 people in the 2009 pandemic, was able to bind to alpha 2-6 receptors in humans very well. The team created four mutations of the HA protein in order to alter it so it could bind to alpha 2-3 receptors even better. They didn’t think that the mutated viruses would spread, but they did, and just as well as the original. It turns out that the virus experienced a genetic reversion that caused the HA protein to attach to both the alpha 2-6 and 2-3 glycan receptors.

“This is an experimental validation that gain of binding to the 2-6 glycan receptor is critical for aerosol transmission” Sasisekharan, a biological engineer at MIT, said in a news release.

After looking at different sections of the respiratory tract, the researchers found that the genetic reversion were prominently found in the soft palate (located at the back of the roof of the mouth). In fact, 90% of the viruses in the soft palate reverted back to the original form by day three. The next step is to uncover why the majority of the genetic reversion occurs in the soft palate and how it does so. But even still, these findings can help monitor flu strains that could one day cause another pandemic.

The research has even received acknowledgement from outside professionals like Lin-Fa Wang, director of the program in emerging infectious disease at Duke-NUS Graduate Medical School, who says it provides “a new frontier in our fight against future emergency of pandemic influenza viruses.”