PB2-588I Enhances 2009 H1N1 Pandemic Influenza Virus Virulence by Increasing Viral Replication and Exacerbating PB2 Inhibition of Beta Interferon Expression
Identifieur interne : 000693 ( Main/Exploration ); précédent : 000692; suivant : 000694PB2-588I Enhances 2009 H1N1 Pandemic Influenza Virus Virulence by Increasing Viral Replication and Exacerbating PB2 Inhibition of Beta Interferon Expression
Auteurs : Zongzheng Zhao [République populaire de Chine] ; Chenyang Yi [République populaire de Chine] ; Lianzhong Zhao [République populaire de Chine] ; Shengyu Wang [République populaire de Chine] ; Lishan Zhou [République populaire de Chine] ; Yong Hu [République populaire de Chine] ; Wei Zou [République populaire de Chine] ; Huanchun Chen [République populaire de Chine] ; Meilin Jin [République populaire de Chine]Source :
- Journal of Virology [ 0022-538X ] ; 2014.
Abstract
The 2009 pandemic H1N1 influenza virus (pdm/09) is typically mildly virulent in mice. In a previous study, we identified four novel swine isolates of pdm/09 viruses that exhibited high lethality in mice. Comparing the consensus sequences of the PB2 subunit of human isolates of pdm/09 viruses with those of the four swine isolate viruses revealed one consensus mutation: T588I. In this study, we determined that 588T is an amino acid mutation conserved in pdm/09 viruses that was exceedingly rare in previous human influenza isolates. To investigate whether the PB2 with the T5581 mutation (PB2-T558I) has an effect on the increased pathogenicity, we rescued a variant containing PB2-588I (Mex_PB2-588I) in the pdm/09 virus, A/Mexico/4486/2009(H1N1), referred to as Mex_WT (where WT is wild type), and characterized the variant
Url:
DOI: 10.1128/JVI.03024-13
PubMed: 24335306
PubMed Central: 3911566
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>The 2009 pandemic H1N1 influenza virus (pdm/09) is typically mildly virulent in mice. In a previous study, we identified four novel swine isolates of pdm/09 viruses that exhibited high lethality in mice. Comparing the consensus sequences of the PB2 subunit of human isolates of pdm/09 viruses with those of the four swine isolate viruses revealed one consensus mutation: T588I. In this study, we determined that 588T is an amino acid mutation conserved in pdm/09 viruses that was exceedingly rare in previous human influenza isolates. To investigate whether the PB2 with the T5581 mutation (PB2-T558I) has an effect on the increased pathogenicity, we rescued a variant containing PB2-588I (Mex_PB2-588I) in the pdm/09 virus, A/Mexico/4486/2009(H1N1), referred to as Mex_WT (where WT is wild type), and characterized the variant <italic>in vitro</italic>
and <italic>in vivo</italic>
. The results indicated that the mutation significantly enhanced polymerase activity in mammalian cells, and the variant exhibited increased growth properties and induced significant weight loss in a mouse model compared to the wild type. We determined that the mutation exacerbated PB2 inhibition of mitochondrial antiviral signaling protein (MAVS)-mediated beta interferon (IFN-β) expression, and PB2-588I was observed to bind to MAVS more efficiently than PB2-588T. The variant induced lower levels of host IFN-β expression than the WT strain during infection. These findings indicate that the pdm/09 influenza virus has increased pathogenicity upon the acquisition of the PB2-T588I mutation and highlight the need for the continued surveillance of the genetic variation of molecular markers in influenza viruses because of their potential effects on pathogenicity and threats to human health.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Hubei</li>
</region>
<settlement><li>Wuhan</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Zhao, Zongzheng" sort="Zhao, Zongzheng" uniqKey="Zhao Z" first="Zongzheng" last="Zhao">Zongzheng Zhao</name>
</region>
<name sortKey="Chen, Huanchun" sort="Chen, Huanchun" uniqKey="Chen H" first="Huanchun" last="Chen">Huanchun Chen</name>
<name sortKey="Chen, Huanchun" sort="Chen, Huanchun" uniqKey="Chen H" first="Huanchun" last="Chen">Huanchun Chen</name>
<name sortKey="Hu, Yong" sort="Hu, Yong" uniqKey="Hu Y" first="Yong" last="Hu">Yong Hu</name>
<name sortKey="Hu, Yong" sort="Hu, Yong" uniqKey="Hu Y" first="Yong" last="Hu">Yong Hu</name>
<name sortKey="Jin, Meilin" sort="Jin, Meilin" uniqKey="Jin M" first="Meilin" last="Jin">Meilin Jin</name>
<name sortKey="Jin, Meilin" sort="Jin, Meilin" uniqKey="Jin M" first="Meilin" last="Jin">Meilin Jin</name>
<name sortKey="Wang, Shengyu" sort="Wang, Shengyu" uniqKey="Wang S" first="Shengyu" last="Wang">Shengyu Wang</name>
<name sortKey="Wang, Shengyu" sort="Wang, Shengyu" uniqKey="Wang S" first="Shengyu" last="Wang">Shengyu Wang</name>
<name sortKey="Yi, Chenyang" sort="Yi, Chenyang" uniqKey="Yi C" first="Chenyang" last="Yi">Chenyang Yi</name>
<name sortKey="Yi, Chenyang" sort="Yi, Chenyang" uniqKey="Yi C" first="Chenyang" last="Yi">Chenyang Yi</name>
<name sortKey="Zhao, Lianzhong" sort="Zhao, Lianzhong" uniqKey="Zhao L" first="Lianzhong" last="Zhao">Lianzhong Zhao</name>
<name sortKey="Zhao, Lianzhong" sort="Zhao, Lianzhong" uniqKey="Zhao L" first="Lianzhong" last="Zhao">Lianzhong Zhao</name>
<name sortKey="Zhao, Zongzheng" sort="Zhao, Zongzheng" uniqKey="Zhao Z" first="Zongzheng" last="Zhao">Zongzheng Zhao</name>
<name sortKey="Zhou, Lishan" sort="Zhou, Lishan" uniqKey="Zhou L" first="Lishan" last="Zhou">Lishan Zhou</name>
<name sortKey="Zhou, Lishan" sort="Zhou, Lishan" uniqKey="Zhou L" first="Lishan" last="Zhou">Lishan Zhou</name>
<name sortKey="Zou, Wei" sort="Zou, Wei" uniqKey="Zou W" first="Wei" last="Zou">Wei Zou</name>
<name sortKey="Zou, Wei" sort="Zou, Wei" uniqKey="Zou W" first="Wei" last="Zou">Wei Zou</name>
</country>
</tree>
</affiliations>
</record>
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