Here's How the Flu Virus Evolves Airborne Transmissibility and Cause Global Outbreaks

by Bidita Debnath on  September 24, 2015 at 6:45 PM Research News
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Scientists from MIT and the National Institute of Allergy and Infectious Diseases (NIAID) have revealed how flu viruses gain the ability to spread. Flu viruses come in many strains, and some are better equipped than others to spread from person to person.
 Here's How the Flu Virus Evolves Airborne Transmissibility and Cause Global Outbreaks
Here's How the Flu Virus Evolves Airborne Transmissibility and Cause Global Outbreaks

Researchers have now discovered that the soft palate -- the soft tissue at the back of the roof of the mouth -- plays a key role in viruses' ability to travel through the air from one person to another. The findings should help scientists better understand how the flu virus evolves airborne transmissibility and assist them in monitoring the emergence of strains with potential to cause global outbreaks.

Researchers made the surprising finding while examining the H1N1 flu strain, which caused a 2009 pandemic that killed more than 250,000 people. Ram Sasisekharan, one of the study's senior authors, has previously shown that airborne transmissibility depends on whether a virus' hemagglutinin (HA) protein can bind to a specific type of receptor on the surface of human respiratory cells.

Some flu viruses bind better to alpha 2-6 glycan receptors, which are found primarily in humans and other mammals, while other viruses are better adapted to alpha 2-3 glycan receptors, found predominantly in birds. The 2009 strain was very good at binding to human alpha 2-6 receptors. In the new study, the researchers made four mutations in the HA molecule of this virus, which made it better suited to bind alpha 2-3 receptors instead of alpha 2-6.

They then used it to infect ferrets, which are often used to model human influenza infection. The researchers believed the mutated virus would not spread, but to their surprise, it traveled through the air just as well as the original version of the virus. After sequencing the virus' genetic material, they found that it had undergone a genetic reversion that allowed its HA protein to bind to alpha 2-6 glycan receptors as well as alpha 2-3 glycan receptors.

The researchers then examined tissue from different parts of the respiratory tract and found that viruses with the genetic reversion were most abundant in the soft palate. By three days after the initial infection, 90 percent of the viruses in this region had the reverted form of the virus. Other sites in the respiratory tract had a mix of the two types of virus. The study appears online in Nature.

Source: ANI

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