H7N9, influenza, receptor binding specificity, mutation, HA gene
A novel avian-origin H7N9 influenza virus was discovered in March in China and has caused a total of 131 people infected including 39 deaths in China as of June 9, 2013. Adaptation of avian viruses to efficiently infect humans requires the viral hemagglutinin (HA) binding switches from avian to human type receptors with help of some mutations in HA. As such it is critical for pandemic assessment to discover these mutations as hallmarks of adaptation. To continue our previous study of this novel H7N9 virus, we identified two sets of mutations in HA. The first set of mutations are present in the current circulating strains of 2013 H7N9 in China, and the second set are potential mutations that were found when compared to the HAs of previous human H7 subtype. These two sets of mutations exhibited unique features. The first group of mutations, on average, enhanced the HA binding to human type receptors whereas reduced that to avian types. Further the reduction of avian binding was almost three times of the increase of the human binding. The second group increased the binding to both human and avian types. But the increase in human types was almost three times of that in the avian types. Though different in their way of changing the binding preference, these two sets of mutations both contained more mutations to decrease the avian binding and increase the human binding than those that did the opposite. Our research highlighted the pandemic potential of this novel virus by showing the important mutations that could potentially help it to adapt to human hosts. Our findings offered new insights into the current state of evolution of this virus, which might be helpful for the continued surveillance of the emergence of H7N9 strains having the ability of human-to-human transmission.
Tsinghua University Press
Wei Hu. Mutations in Hemagglutinin of a Novel Avian-Origin H7N9 Virus That Are Critical for Receptor Binding Specificity. Tsinghua Science and Technology 2013, 18(5): 522-529.