detected in Europe and elsewhere worldwide.2 Gao and colleagues
reported that the H7N9 viruses identified in the first
three patients were of avian origin and all the internal gene
segments were closely related to A/brambling/Beijing/16/
2012-like viruses (H9N2). The neuraminidase (NA) gene was
closely related to A/wild bird/Korea/A14/2011 (H7N9, subtype
KO14) and the gene encoding hemagglutinin (HA) shared
the highest identity with A/duck/ Zhejiang/12/2011(H7N3,
subtype ZJ12).9 The affinity of the influenza virus to different
sialyl-sugar structures is an important determinant of range
and pathogenicity in the viral host.10,11 Q226L in the HA
protein, which was first reported in H7 field viruses, as well as
H5 subtypes, was expected to bind strongly to alpha 2-6
human like receptors.9 Researchers reported that a laboratorygenerated
Q226L mutation at the 210-loop of HA could
change the receptor binding of avian origin to a human-type
receptor binding and might increase the ability of the virus
to be transmitted by air.12,13 Since human influenza viruses
preferentially bind to alpha 2-6 receptors, they might have
greater ability to infect mammalian species.1