Association of Increased Receptor-Binding Avidity of Influenza A(H9N2) Viruses with Escape from Antibody-Based Immunity and Enhanced Zoonotic Potential
Joshua E. Sealy, Tahir Yaqub, Thomas P. Peacock1
, Pengxiang Chang, Burcu Ermetal, Anabel Clements, Jean-Remy Sadeyen, Arslan Mehboob2
, Holly Shelton, Juliet E. Bryant, Rod S. Daniels, John W. McCauley, Munir Iqbal
, and Jean-Remy Royal Veterinary CollegeLondonUKSadeyen
Author affiliations: The Pirbright Institute, Pirbright, UK (J.E. Sealy, T.P. Peacock, P. Chang, A. Clements, J.-R. Sadeyen, H. Shelton, M. Iqbal); University of Veterinary and Animal Sciences, Lahore, Pakistan (T. Yaqub, A. Mehboob); The Francis Crick Institute, London (B. Ermetal, R.S. Daniels, J.W. McCauley); Fondation Mérieux, Lyon, France (J.E. Bryant)
Figure 1. Genotypes of influenza A(H9N2) viruses from Pakistan. Full-genome sequences of 43 contemporary H9N2 avian influenza viruses from Pakistan were used to generate 7 unique genotypes, designated PK1–PK7. Each circle represents a genotype, and n values indicate the total number of viruses assigned to the given genotype. Each line within a circle represents a virus gene segment, and different segment colors between the same gene correspond to a >2% nucleotide difference. Black indicates wild-type virus genes; red, green, and purple indicate mutated genes. HA, hemagglutinin; M, matrix; NA, neuraminidase; NP, nucleoprotein; NS, nonstructural; PA, polymerase acidic; PB, polymerase basic.
Page created: December 18, 2018
Page updated: December 18, 2018
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