The flu strain H7N9 normally affects birds, but is known to have infected at least 1500 people in outbreaks linked to poultry markets in China. The virus is not easily transmitted between people, but the high mortality rate – 40 percent of infections are fatal – means that mutations allowing the virus to spread more easily in humans could have significant consequences for public health.
'We need to know what the virus could do in nature, so we can be alert and aware if we start seeing these changes', said Professor James Paulson of The Scripps Research Institute in California, who led the research published this week in PLOS Pathogens.
The researchers analysed mutations that might occur naturally in the H7N9 genome. In particular, they focused on a protein called H7 hemagglutanin found on the surface of the virus, which binds to receptors in the cells that it infects.
In avian flu, this protein attaches to a bird-specific receptor, which differs from the receptor found in human cells. This means that the virus cannot attach readily, and so the strain of flu does not easily infect people.
Professor Paulson and his team did not directly alter the virus itself. Instead, they identified three small mutations that could make the hemagglutanin protein fragment bind more strongly to human-specific receptors than to receptors in bird cells. It is possible that avian flu with this changed structure of hemagglutanin could infect human cells much more easily, and lead to a strain that could pass from human to human.
However, the likelihood of the H7N9 virus mutating in this specific way is very low.
'These mutations that we've identified haven't occurred. Maybe it's because there are three of them,' Professor Paulson said. 'It's very easy for a virus to make a single mutation, and two is much more difficult. We take some comfort in the fact that it took three mutations to really make the transformation.'
For safety reasons, mutations to complete flu viruses cannot be carried out experimentally in federally-funded research under a White House moratorium, and so how the mutated form of the virus would actually infect and transmit in humans is not known.
'Changes which allow a virus to attach to human cells on their own might not be sufficient to allow the virus to replicate and transmit in humans,' said Dr Fiona Culley, spokesperson for the British Society for Immunology, who was not involved in the study. 'Other additional changes to the virus would probably be needed to allow it to be fully compatible with the machinery of human cells.'