As the UK Covid inquiry considers how well the country planned for and responded to the coronavirus pandemic which swept the globe in 2020, scientists are looking for clues that could help us spot future viral threats.

One of the likeliest avenues will be a zoonotic "spillover" event, where a virus jumps from animals into humans.

This does not necessarily mean that the virus can then spread from human-to-human, but several previous human pandemics have originated in animals such birds, bats, camels and pigs.

Researchers in Glasgow have now identified a gene that could play an important role in viral surveillance.

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What have we learned?

Scientists at Glasgow University's Centre for Virus (CVR) have identified the human gene, BTN3A3, as playing a key role in protecting humans against avian flu.

Although it is not the only gene involved in coding for an immune defence against strains of bird flu, it is the first time that the role of BTN3A3 has been identified.

Through a series of tests, the study team were able to show that the BTN3A3 gene blocks the replication of avian flu in human cells in the respiratory tract.

What about 'spillover' events?

The scientists wanted to understand why some humans do become infected with strains of 'bird flu'.

They discovered that some strains of avian flu viruses have developed mutations which enable them to 'escape' the blocking effects of BTN3A3.

This includes the H7N9 strain, which has infected more than 1,500 people since 2013 with a case-fatality rate of 40%.

The team analysed avian-isolated H7N9 sequences deposited at the Global Initiative on Sharing All Influenza Data (GISAID).

Before 2013, they found that only 14% (seven out of 50 samples) carried BTN3A3-resistant mutations. From 2013 onwards, however, this rose to 93.5%.

Analysis of isolates of the H5N1 strain which is currently in circulation and responsible for millions of birds' deaths shows that around 50% of samples are BTN3A3-resistant.

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Why is this important?

At the moment there is no evidence of human-to-human transmission of H5N1 infections.

However, past pandemics show us that the first step is when viruses find a way to leap from animals into humans.

The original SARS (Severe acute respiratory syndrome) outbreak in 2002 was traced to a colony of bats, while MERS (Middle East respiratory syndrome) is believed to have spread to humans from camels.

Scientists want to use genomic surveillance to identify potential threats at an early stage.

That means they have to know which genes are involved in resistance, and which viral strains are displaying mutations that confer resistance.

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What about past pandemics?

By tracking past human influenza pandemics - including the devastating 1918-19 Spanish flu pandemic, thwe 1957 Asian flu, 1968 Hong Kong flu, and the 2009 swine flu pandemic - the researchers showed that they were all caused by influenza viruses that were resistant to BTN3A3.

This suggests that having resistance to this gene may be a key factor in whether any flu strain has human pandemic potential.