Author(s)： Wei Hu
The advent of a novel avian origin H7N9 emerged in China in March 2013 is of major health concern, as it has little virulence in birds but can cause severe illness and death in humans. As people continue to get infected by this new virus in 2014, we need to understand the current status and trend of its evolution at the end of year 2014. The influenza viruses have two surface proteins, haemagglutinin (HA) and neuraminidase (NA), which are involved in viral entry into and egress from the host cells respectively. In a previous study published in May 2013, we found that the HA protein of this new human H7N9 virus was able to preferentially bind to the avian type receptors as its primary binding and human type receptors as its secondary, which was confirmed by several web lab experiments a few months later in 2013. The current study examined the binding preference of human H7N9 again trying to uncover any change in the HA binding properties as this virus ran its course from 2013 to 2014. Our analysis concluded that the HA binding patterns of this novel virus were stable and similar to avian H7N9 in Asia and in Europe until August 2013, but after that time the virus gradually started to change and exhibit enhanced binding features of avian H7N9 in North America. Further investigation of the observed change identified a few positions in HA that could be potentially important for distinguishing the HA sequences of human H7N9 in China collected before and after August 2013. As a result, we discovered a single amino acid substitution R47K in HA that was believed to be the primary cause for this shift of binding patterns. Finally, our findings also implied that the human infections with H7N9 in China in 2013 were more likely caused by chickens than by ducks.
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