Three mutations switch H7N9 influenza to human-type receptor specificity.
Robert P de Vries, Wenjie Peng, Oliver C Grant, Andrew J Thompson, Xueyong Zhu, Kim M Bouwman, Alba T Torrents de la Pena, Marielle J van Breemen, Iresha N Ambepitiya Wickramasinghe, Cornelis AM de Haan, Wenli Yu, Ryan McBride, Rogier W Sanders, Robert J Woods, Monique H Verheije, Ian A Wilson, James C Paulson
PLoS Pathogens | Published : 2017
The avian H7N9 influenza outbreak in 2013 resulted from an unprecedented incidence of influenza transmission to humans from infected poultry. The majority of human H7N9 isolates contained a hemagglutinin (HA) mutation (Q226L) that has previously been associated with a switch in receptor specificity from avian-type (NeuAcα2-3Gal) to human-type (NeuAcα2-6Gal), as documented for the avian progenitors of the 1957 (H2N2) and 1968 (H3N2) human influenza pandemic viruses. While this raised concern that the H7N9 virus was adapting to humans, the mutation was not sufficient to switch the receptor specificity of H7N9, and has not resulted in sustained transmission in humans. To determine if the H7 HA ..View full abstract
Awarded by NIAID NIH HHS
Awarded by NIGMS NIH HHS
Awarded by NCI NIH HHS