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Autophagy induced by infectious pancreatic necrosis virus promotes its multiplication in the Chinook salmon embryo cell line CHSE-214.

Identifieur interne : 000146 ( Main/Exploration ); précédent : 000145; suivant : 000147

Autophagy induced by infectious pancreatic necrosis virus promotes its multiplication in the Chinook salmon embryo cell line CHSE-214.

Auteurs : Ying Dong [République populaire de Chine] ; Jingzhuang Zhao [République populaire de Chine] ; Xiaoyu Chen [République populaire de Chine] ; Miao Liu [République populaire de Chine] ; Guangming Ren [République populaire de Chine] ; Tongyan Lu [République populaire de Chine] ; Yizhi Shao [République populaire de Chine] ; Liming Xu [République populaire de Chine]

Source :

RBID : pubmed:31874298

Descripteurs français

English descriptors

Abstract

Infectious pancreatic necrosis virus (IPNV) is a common pathogen that causes huge economic losses for the salmonid aquaculture industry. Autophagy plays an important regulatory role in the invasion of pathogenic microorganisms. In this study, we explored the relationship between IPNV infection and autophagy in Chinook salmon embryo (CHSE-214) cells using standard methods. Transmission electron microscopy showed that IPNV infection produced typical structures of autophagosomes in CHSE-214 cells. Transformation of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II protein, a marker of autophagy, was observed in IPNV-infected cells using confocal fluorescence microscopy and western blot analysis. Western blotting also showed that expression of the autophagy substrate p62 was significantly decreased in IPNV-infected cells. The influence of autophagy on IPNV multiplication was further clarified with cell culture experiments using autophagy inducer rapamycin and autophagy inhibitor 3-methyladenine. Rapamycin promoted IPNV multiplication at both the nucleic acid and protein levels, which led to higher IPNV yields; 3-methyladenine treatment had the opposite effect. This study has demonstrated that IPNV can induce autophagy, and that autophagy promotes the multiplication of IPNV in CHSE-214 cells.

DOI: 10.1016/j.fsi.2019.12.067
PubMed: 31874298


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">Infectious pancreatic necrosis virus (IPNV) is a common pathogen that causes huge economic losses for the salmonid aquaculture industry. Autophagy plays an important regulatory role in the invasion of pathogenic microorganisms. In this study, we explored the relationship between IPNV infection and autophagy in Chinook salmon embryo (CHSE-214) cells using standard methods. Transmission electron microscopy showed that IPNV infection produced typical structures of autophagosomes in CHSE-214 cells. Transformation of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II protein, a marker of autophagy, was observed in IPNV-infected cells using confocal fluorescence microscopy and western blot analysis. Western blotting also showed that expression of the autophagy substrate p62 was significantly decreased in IPNV-infected cells. The influence of autophagy on IPNV multiplication was further clarified with cell culture experiments using autophagy inducer rapamycin and autophagy inhibitor 3-methyladenine. Rapamycin promoted IPNV multiplication at both the nucleic acid and protein levels, which led to higher IPNV yields; 3-methyladenine treatment had the opposite effect. This study has demonstrated that IPNV can induce autophagy, and that autophagy promotes the multiplication of IPNV in CHSE-214 cells.</div>
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<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D000071182" MajorTopicYN="N">Autophagosomes</DescriptorName>
<QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018175" MajorTopicYN="N">Birnaviridae Infections</DescriptorName>
<QualifierName UI="Q000662" MajorTopicYN="Y">veterinary</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004625" MajorTopicYN="N">Embryo, Nonmammalian</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005393" MajorTopicYN="N">Fish Diseases</DescriptorName>
<QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018061" MajorTopicYN="N">Infectious pancreatic necrosis virus</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D046529" MajorTopicYN="N">Microscopy, Electron, Transmission</DescriptorName>
<QualifierName UI="Q000662" MajorTopicYN="N">veterinary</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D012474" MajorTopicYN="Y">Salmon</DescriptorName>
<QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D014779" MajorTopicYN="Y">Virus Replication</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Autophagy</Keyword>
<Keyword MajorTopicYN="N">Chinook salmon embryo cells (CHSE-214)</Keyword>
<Keyword MajorTopicYN="N">Infectious pancreatic necrosis virus (IPNV)</Keyword>
<Keyword MajorTopicYN="N">LC3</Keyword>
<Keyword MajorTopicYN="N">p62</Keyword>
</KeywordList>
<CoiStatement>Declaration of competing interest All authors declare that no conflicts of interest exist.</CoiStatement>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2019</Year>
<Month>08</Month>
<Day>17</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised">
<Year>2019</Year>
<Month>12</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2019</Year>
<Month>12</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2019</Year>
<Month>12</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2020</Year>
<Month>9</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2019</Year>
<Month>12</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">31874298</ArticleId>
<ArticleId IdType="pii">S1050-4648(19)31196-9</ArticleId>
<ArticleId IdType="doi">10.1016/j.fsi.2019.12.067</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Dong, Ying" sort="Dong, Ying" uniqKey="Dong Y" first="Ying" last="Dong">Ying Dong</name>
</noRegion>
<name sortKey="Chen, Xiaoyu" sort="Chen, Xiaoyu" uniqKey="Chen X" first="Xiaoyu" last="Chen">Xiaoyu Chen</name>
<name sortKey="Liu, Miao" sort="Liu, Miao" uniqKey="Liu M" first="Miao" last="Liu">Miao Liu</name>
<name sortKey="Lu, Tongyan" sort="Lu, Tongyan" uniqKey="Lu T" first="Tongyan" last="Lu">Tongyan Lu</name>
<name sortKey="Ren, Guangming" sort="Ren, Guangming" uniqKey="Ren G" first="Guangming" last="Ren">Guangming Ren</name>
<name sortKey="Shao, Yizhi" sort="Shao, Yizhi" uniqKey="Shao Y" first="Yizhi" last="Shao">Yizhi Shao</name>
<name sortKey="Xu, Liming" sort="Xu, Liming" uniqKey="Xu L" first="Liming" last="Xu">Liming Xu</name>
<name sortKey="Zhao, Jingzhuang" sort="Zhao, Jingzhuang" uniqKey="Zhao J" first="Jingzhuang" last="Zhao">Jingzhuang Zhao</name>
</country>
</tree>
</affiliations>
</record>

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