Assessment of the Internal Genes of Influenza A (H7N9) Virus Contributing to High Pathogenicity in Mice
Identifieur interne : 000A89 ( Ncbi/Checkpoint ); précédent : 000A88; suivant : 000A90Assessment of the Internal Genes of Influenza A (H7N9) Virus Contributing to High Pathogenicity in Mice
Auteurs : Yuhai Bi [République populaire de Chine] ; Qing Xie [République populaire de Chine] ; Shuang Zhang [République populaire de Chine] ; Yun Li [République populaire de Chine] ; Haixia Xiao [République populaire de Chine] ; Tao Jin [République populaire de Chine] ; Weinan Zheng [République populaire de Chine] ; Jing Li [République populaire de Chine] ; Xiaojuan Jia [République populaire de Chine] ; Lei Sun [République populaire de Chine] ; Jinhua Liu [République populaire de Chine] ; Chuan Qin [République populaire de Chine] ; George F. Gao [République populaire de Chine] ; Wenjun Liu [République populaire de Chine]Source :
- Journal of Virology [ 0022-538X ] ; 2014.
Abstract
The recently identified H7N9 influenza A virus has caused severe economic losses and worldwide public concern. Genetic analysis indicates that its six internal genes all originated from H9N2 viruses. However, the H7N9 virus is more highly pathogenic in humans than H9N2, which suggests that the internal genes of H7N9 have mutated. To analyze which H7N9 virus internal genes contribute to its high pathogenicity, a series of reassortants was generated by reverse genetics, with each virus containing a single internal gene of the typical A/Anhui/1/2013 (H7N9) (AH-H7N9) virus in the genetic background of the A/chicken/Shandong/lx1023/2007 (H9N2) virus. The replication ability, polymerase activity, and pathogenicity of these viruses were then evaluated
Url:
DOI: 10.1128/JVI.02390-14
PubMed: 25320305
PubMed Central: 4301103
Affiliations:
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<series><title level="j">Journal of Virology</title>
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<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<p>The recently identified H7N9 influenza A virus has caused severe economic losses and worldwide public concern. Genetic analysis indicates that its six internal genes all originated from H9N2 viruses. However, the H7N9 virus is more highly pathogenic in humans than H9N2, which suggests that the internal genes of H7N9 have mutated. To analyze which H7N9 virus internal genes contribute to its high pathogenicity, a series of reassortants was generated by reverse genetics, with each virus containing a single internal gene of the typical A/Anhui/1/2013 (H7N9) (AH-H7N9) virus in the genetic background of the A/chicken/Shandong/lx1023/2007 (H9N2) virus. The replication ability, polymerase activity, and pathogenicity of these viruses were then evaluated <italic>in vitro</italic>
and <italic>in vivo</italic>
. These recombinants displayed high genetic compatibility, and the H7N9-derived PB2, M, and NP genes were identified as the virulence genes for the reassortants in mice. Further investigation confirmed that the PB2 K627 residue is critical for the high pathogenicity of the H7N9 virus and the reassortant containing the H7N9-derived PB2 segment (H9N2-AH/PB2). Notably, the H7N9-derived PB2 gene displayed greater compatibility with the H9N2 genome than that of H7N9, endowing the H9N2-AH/PB2 reassortant with greater viability and virulence than the parental H7N9 virus. In addition, the H7N9 virus, with the exception of the H9N2 reassortants, could effectively replicate in human A549 cells. Our results indicate that PB2, M, and NP are the key virulence genes, together with the surface hemagglutinin (HA) and neuraminidase (NA) proteins, contributing to the high infectivity of the H7N9 virus in humans.
</p>
<p><bold>IMPORTANCE</bold>
To date, the novel H7N9 influenza A virus has caused 437 human infections, with approximately 30% mortality. Previous work has primarily focused on the two viral surface proteins, HA and NA, but the contribution of the six internal genes to the high pathogenicity of H7N9 has not been systematically studied. Here, the H9N2 virus was used as a genetic backbone to evaluate the virulence genes of H7N9 virus <italic>in vitro</italic>
and <italic>in vivo</italic>
. Our data indicate that the PB2, M, and NP genes play important roles in viral infection in mice and, together with HA and NA, contribute to the high infectivity of the H7N9 virus in humans.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Guangdong</li>
</region>
<settlement><li>Pékin</li>
<li>Shenzhen</li>
<li>Tianjin</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Bi, Yuhai" sort="Bi, Yuhai" uniqKey="Bi Y" first="Yuhai" last="Bi">Yuhai Bi</name>
</noRegion>
<name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
<name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
<name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
<name sortKey="Gao, George F" sort="Gao, George F" uniqKey="Gao G" first="George F." last="Gao">George F. Gao</name>
<name sortKey="Jia, Xiaojuan" sort="Jia, Xiaojuan" uniqKey="Jia X" first="Xiaojuan" last="Jia">Xiaojuan Jia</name>
<name sortKey="Jin, Tao" sort="Jin, Tao" uniqKey="Jin T" first="Tao" last="Jin">Tao Jin</name>
<name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name>
<name sortKey="Li, Yun" sort="Li, Yun" uniqKey="Li Y" first="Yun" last="Li">Yun Li</name>
<name sortKey="Liu, Jinhua" sort="Liu, Jinhua" uniqKey="Liu J" first="Jinhua" last="Liu">Jinhua Liu</name>
<name sortKey="Liu, Wenjun" sort="Liu, Wenjun" uniqKey="Liu W" first="Wenjun" last="Liu">Wenjun Liu</name>
<name sortKey="Qin, Chuan" sort="Qin, Chuan" uniqKey="Qin C" first="Chuan" last="Qin">Chuan Qin</name>
<name sortKey="Sun, Lei" sort="Sun, Lei" uniqKey="Sun L" first="Lei" last="Sun">Lei Sun</name>
<name sortKey="Xiao, Haixia" sort="Xiao, Haixia" uniqKey="Xiao H" first="Haixia" last="Xiao">Haixia Xiao</name>
<name sortKey="Xie, Qing" sort="Xie, Qing" uniqKey="Xie Q" first="Qing" last="Xie">Qing Xie</name>
<name sortKey="Xie, Qing" sort="Xie, Qing" uniqKey="Xie Q" first="Qing" last="Xie">Qing Xie</name>
<name sortKey="Zhang, Shuang" sort="Zhang, Shuang" uniqKey="Zhang S" first="Shuang" last="Zhang">Shuang Zhang</name>
<name sortKey="Zheng, Weinan" sort="Zheng, Weinan" uniqKey="Zheng W" first="Weinan" last="Zheng">Weinan Zheng</name>
</country>
</tree>
</affiliations>
</record>
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