Identification of a viral determinant of H7N9 pathogenesis.
A novel avian H7N9 influenza A virus emerged in East China in 2013 to cause zoonotic human disease associated with significant mortality. Chris MOK’s lab, which is working on the identification of viral genetic markers of mammalian adaptation and disease severity of avian influenza, has found some initial clues to understand how H7N9 is jumping into humans. Chris focused on the polymerase basic protein 2 (PB2) gene, since many human (but not avian) H7N9 virus isolates have an amino acid substitution at position E627K. With his team (Mr Horace LEE, Research Assistant and Mr Maxime LESTRA, Volontaire International), he investigated the role of this and other functionally related mutations, for polymerase activity in vitro, virus replication competence and pathogenicity in the mouse model. They found that E627K and functional related mutations are associated with increased polymerase activity, increased viral replication competence and increased disease severity in mice.
This work entitled "Amino Acid Substitutions in Polymerase Basic Protein 2 Gene Contribute to the Pathogenicity of the Novel A/H7N9 Influenza Virus in Mammalian Hosts" has been published in Journal of Virology.