Scientists discover flu breeds in the roof of the mouth

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Virus breeds in soft palate, which separates back of mouth and nasal cavity
Palate also plays a key role in the virus's ability to travel through the air
The findings could help identify how flu is transmitted from human to human - and predict which viruses are most likely to spark pandemics

Published: 09:35 EST, 24 September 2015 | Updated: 15:42 EST, 24 September 2015

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The soft tissue that separates the back of the mouth and the nasal cavity - plays a key role in the flu virus's ability to travel through the air

Scientists have discovered that flu breeds in the roof of the mouth, explaining why coughs and sneezes help the virus spread.

They found the soft palate - the soft tissue that separates the back of the mouth and the nasal cavity - plays a key role in the virus's ability to travel through the air from one person to another.

Flu viruses come in many strains, and some are better equipped than others to spread.

The findings could help identify how flu is transmitted from human to human and predict which strains are most likely to spark pandemics.

The theory is the flu viruses more able to travel through the air outcompete other variants in the soft palate.

And inflammation associated with infection in the soft palate stimulates the sneezing and coughing needed to better propel the flu virus out of the mouth.

Dr Kanta Subbarao, of the National Institute of Allergy and Infectious Diseases (NIAID) in the US, said: 'Historically, the soft palate has not been examined in animal models of influenza.'

He added more research was needed to better define the characteristics that make it a key spot for a virus to rapidly evolve and be transmitted.

The study, published online in the journal Nature, was carried out on ferrets, which are often used to model human flu infection.

The scientists found this patch of mucous-coated soft tissue is a key site for the emergence of flu viruses.

Flu infection starts when an influenza virus protein called hemagglutinin binds to sialic acid (SA) molecules on the tops of chain-like proteins that line tissue in the respiratory tract.

Flu viruses adapted to humans and other mammals bind preferentially to a type of SA called alpha 2,6 SA (a2,6 SA).

This is the predominant form found in the upper respiratory tract of mammals, while avian flu viruses bind best to a form, a2,3 SA, that predominates in birds.

Scientists began their research by making four mutations in the hemagglutinin of the flu strain responsible for the 2009 influenza pandemic, a strain notoriously good at spreading from person to person.

The intent of introducing the mutations was to make the virus preferentially bind to bird-type SA and, presumably, be less transmissible via air than the original virus.

They then used the engineered virus to infect a group of ferrets, which are widely used as a model of human influenza infection.

The findings could help identify how flu (pictured) is transmitted from human to human - and also predict which viruses are most likely to spark pandemics

The next day, uninfected ferrets were placed in cages separated from infected ferrets by a perforated barrier. Nasal secretions were collected from all of the animals for two weeks.

Dr Subbarao added: 'To our surprise, the engineered flu virus was transmitted by the airborne route to uninfected ferrets just as well as the original non-mutated virus.'

To understand this unexpected result, the researchers sequenced viral genetic material obtained from the ferret nasal washes.

They discovered that airborne transmission was associated with a single genetic change in the engineered virus's hemagglutinin that gave it the ability to bind to mammalian-type a2,6 SA of a particular class (long chain) without the loss of the other introduced changes that had made it a a2,3 SA binding type.

Subsequently, they passed it on to uninfected ferrets in the adjacent cages.