China bird flu may be two mutations from a pandemic
点击量： 时间：2017-12-11 06:01:10
By Debora MacKenzie IN CHINA, eight people had died and at least 16 more were seriously ill in the latest outbreak of bird flu, H7N9, as New Scientist went to press. But there are fears that the death toll could rise much higher because the virus already has three of the five mutations that we know would allow another bird flu, H5N1, to spread between mammals. No one knows for sure if the five mutations discovered last year by Ron Fouchier and colleagues at Erasmus Medical Centre in Rotterdam, the Netherlands, will do the same thing in H7N9. But we do know that some of the mutations helped viruses from three other flu families go pandemic. Chinese authorities are tracing contacts of known cases to see whether the infection has already spread between humans. Two more people with H7N9 only show mild symptoms, so the authorities are also trying to establish how often it makes people seriously ill. Most recent pandemic viruses have been hybrids of bird and mammalian flu, and therefore relatively mild because mammalian flu tends to be less severe in people than bird flu. Pure bird flu viruses, like H5N1 and H7N9, are potentially more dangerous. The most lethal pandemic we know of, which spread across the world in 1918, was a pure bird flu that acquired mutations that allowed it to spread in humans. Virologists fear H7N9 might be doing that. In recent years, H5N1 has spread widely in birds, but it has not evolved the ability to spread readily between mammals. Fouchier’s work – which came under fire because of fears that it would allow bioterrorists to engineer an H5N1 pandemic – shows that, in principle, it can spread between ferrets, and with no obvious loss of virulence. To get transmissible H5N1, Fouchier first had to prime the virus with three mutations known to adapt bird flu to mammals, then allow the other two requisite mutations to evolve in the animals. Two of the three deliberately added mutations allow the HA surface protein from bird flu in the H5, H2 and H3 families to bind to cells in mammals’ noses. The virus that broke out in 1918 – from the H1 family – had similar mutations with the same effect. Such binding mutations have never been seen in wild H5N1 – but H7N9 already has one of the two. If the H7N9 virus can bind to mammalian cells, it could adapt even further to mammals, just as Fouchier’s primed H5N1 did in his ferret experiments. “If what we know about these mutations in other flu subtypes is also the case for this virus, then it’s already part way there,” says Derek Smith at the University of Cambridge. “That’s why everybody is concerned about this.” The virus also has a second of Fouchier’s mutations in a polymerase protein which allows the powerful replicating enzyme that makes bird flu so virulent to work at mammalian temperatures. This mutation has been present in all pandemic viruses. The third mutation in H7N9, which led to the spread of H5N1 in Fouchier’s work, removes a sugar group from HA. That leaves only two more mutations, both in HA, before this H7N9 has Fouchier’s five. “All pandemic viruses have acquired this [mammalian cell] binding and polymerase activity,” says Fouchier. “The H7N9 has these characteristics. So the question is, what else does it need – if anything?