In May the World Health Organisation (WHO) confirmed 26 cases of avian influenza in humans. The cases all stemmed from China, and while most were people who had been in contact with live poultry, two were not.
It is those last two cases that set off alarm bells for public health authorities around the world, because it is possible they contracted the virus – known as H7N9 – from another human.
At present, few cases of human-to-human H7N9 transmission have ever been recorded, and the position of the WHO authorities is that the virus is currently incapable of sustained transmission between people. The very real possibility that it might at some point acquire a mutation that enables easy person-to-person spread is, however, the stuff of epidemiological nightmares.
Understanding exactly how that might happen is now a significant step closer thanks to investigations carried out at The Scripps Research Institute in California, US, and published in the journal PLOS Pathogens.
A team of scientists led by James Paulson looked at mutations that could occur in the genome of H7N9. In particular, they looked at a protein called hemagglutanin, which is found on the surface of all influenza viruses and is known to play a key role in facilitating entry into host cells.
There are several different subtypes of influenza hemagglutanin, numbered H1 to H16. Each has a specific amino acid sequence that allows it to bind to receptors on particular types of cells. Human influenza viruses, for instance, have so far all been found to have hemagglutanin sequences H1, H2 and H3.
In contrast, avian flu viruses have sequences that bind primarily to bird cells. To become capable of person-to-person spread these would have to change structure to allow strong attachment to human tissue.
To see whether this was possible, Paulson and colleagues cultured hemagglutanin in an experimental cell line, identifying and propagating amino acid mutations in the process.
They discovered several different combinations of three amino acid changes that altered the hemagglutanin’s specificity from bird to human cells. A second experiment revealed the mutated protein was capable of latching onto human trachea tissue.
Further experiments, using animals to test how inducing the changes affected H7N9 virulence, were not possible, because safety regulations prohibit inducing such change in actual flu viruses.
Nevertheless, the scientists recommend checking future laboratory-confirmed human avian flu cases to see if any such mutations have occurred in the virus’s hemagglutanin coating.
If it has, they say, it could provide an early warning that the nightmare potential of avian flu is on the brink of being realised.
Andrew Masterson is a former editor of Cosmos.
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