Complete Genome Sequence of an H7N3 Avian Influenza Virus
Isolated from Ducks in Southern China
Peirong Jiao, Liangmeng Wei, Runyu Yuan, Yafen Song, Lan Cao, and Ming Liao
MOA Key Laboratory for Animal Vaccine Development, Key Laboratory of Zoonoses Control and Prevention of Guangdong, College of Veterinary Medicine, South China
Agricultural University, Guangzhou, China
We report here the complete genomic sequence of an H7N3 avian influenza virus (AIV) isolate, which was obtained from
duck in 1996. This is the first report of this subtype of AIV being isolated from duck in Guangdong of Southern China.
Genomic sequence and phylogenetic analyses showed that it was highly homologous with the wild bird virus A/ruddy turn-
stone/Delaware Bay/135/1996 (H7N3) and that all eight genes of this virus belonged to the North America gene pool. The
availability of genome sequences is helpful to further investigations of epidemiology and evolution of AIV between water-
fowl and wild birds.
aminidase (NA) glycoproteins, which are located on the outer
surface of the envelope (5). At present, 17 HA and 9 NA sub-
types have been recognized, and only viruses of H5 and H7
subtypes have been shown to cause highly pathogenic avian
influenza (HPAI) in susceptible species (7, 9, 6). The H7 AIV
caused disease outbreaks in poultry in Europe, North America,
South America, and South Asia and in humans in Europe and
North America (4). In 2003, an epidemic of HPAI A virus sub-
type H7N7 occurred in the Netherlands, the virus was trans-
potential for interspecies transmission. There have been only
limited cases of H7 AIV isolated in China, and the first report
was in 2002 when a routine surveillance was carried out in
poultry in Northern China (4).
In this study, an H7N3 strain, named A/Duck/Guangdong/
1/1996 (H7N3), was first isolated from duck in Guangdong of
sequence with an ABI 3730 genetic analyzer using the Sanger
method, which was based on DNA fragments amplified by PCR
with a previous primer (4). Sequence fragments were assem-
bled using Sequencher 5.0. The complete genome of the strain
consists of eight segments of negative-sense single-stranded
RNA molecules, including PB2, PB1, PA, HA, NP, NA, M, and
NS. The full lengths of each segment are 2,341, 2,341, 2,233,
1,731, 1,565, 1,453, 1,027, and 890 nucleotides, respectively.
The eight genes encode the following proteins with the indi-
NP, 498; NA, 469; M1, 252; M2, 80; NS1, 230; and NS2, 121.
The amino acid sequence at the cleavage site in the HA mole-
cule is PENPKTR2GLF, with the characteristic of low-pathoge-
nicity AIV. An analysis of potential N-glycosylation sites of the
surface proteins indicated that the strain possesses six potential
N-glycosylation sites (positions 30, 46, 141, 421, 493, and 516) in
the HA protein and six (positions 14, 57, 66, 72, 146, and 308)
in the receptor-binding site in the HA protein, findings which
showed that it is avian-origin influenza virus.
vian influenza viruses (AIV) are classified in the family
Orthomyxoviridae, genus Influenzavirus A (1). They are
of this virus belonged to the North America gene pool and were
highly homologous (nucleotide homologies were above 99%)
135/1996 (H7N3). Thus, the virus may be transmitted directly to
ducks from wild birds.
These data are useful for analyses of epidemiology and evolu-
tionary characteristics of AIV between waterfowl and wild birds
and support the idea for more-extensive and long-term AIV sur-
Nucleotide sequence accession numbers. The genome se-
quences of A/Duck/Guangdong/1/1996 (H7N3) have been de-
posited in GenBank under accession numbers JQ988864 to
This work was supported by grants from the Natural Science Foundation
the National Natural Science Foundation of China (no. 31172343),
the Science and Technology Projects of Guangdong Province (no.
University Project of Guangdong Province.
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Received 29 April 2012 Accepted 30 April 2012
Address correspondence to Ming Liao, email@example.com.
P.J. and L.W. contributed equally to this work.
Copyright © 2012, American Society for Microbiology. All Rights Reserved.
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