[Pathogenic effect of pandemic influenza virus H1N1 under replication in cultures of human cells].
Identifieur interne : 001F34 ( PubMed/Checkpoint ); précédent : 001F33; suivant : 001F35[Pathogenic effect of pandemic influenza virus H1N1 under replication in cultures of human cells].
Auteurs : O P Zhirnov ; I V Vorob'Eva ; O A Safonova ; N A Malyshev ; F. Schwalm ; H D KlenkSource :
- Voprosy virusologii [ 0507-4088 ]
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Grippe humaine.
- physiologie : Effet cytopathogène viral, Réplication virale, Sous-type H1N1 du virus de la grippe A.
- épidémiologie : Grippe humaine.
- Animaux, Cellules Caco-2, Cellules rénales canines Madin-Darby, Chiens, Humains, Pandémies.
English descriptors
- KwdEn :
- MESH :
- epidemiology : Influenza, Human.
- metabolism : Influenza, Human.
- physiology : Cytopathogenic Effect, Viral, Influenza A Virus, H1N1 Subtype, Virus Replication.
- Animals, Caco-2 Cells, Dogs, Humans, Madin Darby Canine Kidney Cells, Pandemics.
Abstract
The propagation of the pandemic influenza virus H1N1 in cultures of bronchial (Calu-3) and intestinal (Caco-2) differentiated epithelial cells of human origin was studied. The canine epithelial cell lines, MDCK-H and MDCK-2, were comparatively tested. The two human cell lines were found to be highly sensitive to the influenza pandemic strains A/Hamburg/05/09 and A/Moscow/501/2011 and maintained their replication without addition of trypsin to culture medium. Virus strains of seasonal influenza H1N1, such as A/Moscow/450/2003, A/Memphis/14/96, and laboratory strain A/PR/8/34, multiplied in these human cells in similar manner. The intracellular cleavage HA0-->HA1+HA2 by the host virus-activating protease (IAP) occurred in both human cell lines under infection with each influenza virus H1N1 including pandemic ones. Comparatively, this cleavage of all influenza H1N1 virus strains appeared to be either undetectable or low-detectible in MDCK-H and MDCK-2, respectively, thereby implying low levels of active IAP in these cells. Multiplication of pandemic and seasonal influenza H1N1 viruses in Calu-3 and Caco-2 cells caused cytopathic effect, which was accompanied with low autophagy and apoptosis events. These data allow recommending human cell lines, Calu-3 and Caco-2, for optimized isolation and passaging of clinical strains of Influenza pandemic viruses H1N1.
PubMed: 24354061
Affiliations:
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pubmed:24354061Le document en format XML
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Schwalm</name></author><author><name sortKey="Klenk, H D" sort="Klenk, H D" uniqKey="Klenk H" first="H D" last="Klenk">H D Klenk</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="????"><PubDate><MedlineDate>2013 Jul-Aug</MedlineDate></PubDate></date><idno type="RBID">pubmed:24354061</idno><idno type="pmid">24354061</idno><idno type="wicri:Area/PubMed/Corpus">000903</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000903</idno><idno type="wicri:Area/PubMed/Curation">000903</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000903</idno><idno type="wicri:Area/PubMed/Checkpoint">001F34</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001F34</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[Pathogenic effect of pandemic influenza virus H1N1 under replication in cultures of human cells].</title><author><name sortKey="Zhirnov, O P" sort="Zhirnov, O P" uniqKey="Zhirnov O" first="O P" last="Zhirnov">O P Zhirnov</name></author><author><name sortKey="Vorob Eva, I V" sort="Vorob Eva, I V" uniqKey="Vorob Eva I" first="I V" last="Vorob'Eva">I V Vorob'Eva</name></author><author><name sortKey="Safonova, O A" sort="Safonova, O A" uniqKey="Safonova O" first="O A" last="Safonova">O A Safonova</name></author><author><name sortKey="Malyshev, N A" sort="Malyshev, N A" uniqKey="Malyshev N" first="N A" last="Malyshev">N A Malyshev</name></author><author><name sortKey="Schwalm, F" sort="Schwalm, F" uniqKey="Schwalm F" first="F" last="Schwalm">F. Schwalm</name></author><author><name sortKey="Klenk, H D" sort="Klenk, H D" uniqKey="Klenk H" first="H D" last="Klenk">H D Klenk</name></author></analytic><series><title level="j">Voprosy virusologii</title><idno type="ISSN">0507-4088</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Caco-2 Cells</term><term>Cytopathogenic Effect, Viral (physiology)</term><term>Dogs</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype (physiology)</term><term>Influenza, Human (epidemiology)</term><term>Influenza, Human (metabolism)</term><term>Madin Darby Canine Kidney Cells</term><term>Pandemics</term><term>Virus Replication (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules Caco-2</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Effet cytopathogène viral (physiologie)</term><term>Grippe humaine (métabolisme)</term><term>Grippe humaine (épidémiologie)</term><term>Humains</term><term>Pandémies</term><term>Réplication virale (physiologie)</term><term>Sous-type H1N1 du virus de la grippe A (physiologie)</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Effet cytopathogène viral</term><term>Réplication virale</term><term>Sous-type H1N1 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cytopathogenic Effect, Viral</term><term>Influenza A Virus, H1N1 Subtype</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Caco-2 Cells</term><term>Dogs</term><term>Humans</term><term>Madin Darby Canine Kidney Cells</term><term>Pandemics</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules Caco-2</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Humains</term><term>Pandémies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The propagation of the pandemic influenza virus H1N1 in cultures of bronchial (Calu-3) and intestinal (Caco-2) differentiated epithelial cells of human origin was studied. The canine epithelial cell lines, MDCK-H and MDCK-2, were comparatively tested. The two human cell lines were found to be highly sensitive to the influenza pandemic strains A/Hamburg/05/09 and A/Moscow/501/2011 and maintained their replication without addition of trypsin to culture medium. Virus strains of seasonal influenza H1N1, such as A/Moscow/450/2003, A/Memphis/14/96, and laboratory strain A/PR/8/34, multiplied in these human cells in similar manner. The intracellular cleavage HA0-->HA1+HA2 by the host virus-activating protease (IAP) occurred in both human cell lines under infection with each influenza virus H1N1 including pandemic ones. Comparatively, this cleavage of all influenza H1N1 virus strains appeared to be either undetectable or low-detectible in MDCK-H and MDCK-2, respectively, thereby implying low levels of active IAP in these cells. Multiplication of pandemic and seasonal influenza H1N1 viruses in Calu-3 and Caco-2 cells caused cytopathic effect, which was accompanied with low autophagy and apoptosis events. These data allow recommending human cell lines, Calu-3 and Caco-2, for optimized isolation and passaging of clinical strains of Influenza pandemic viruses H1N1.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24354061</PMID><DateCompleted><Year>2014</Year><Month>01</Month><Day>17</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0507-4088</ISSN><JournalIssue CitedMedium="Print"><Volume>58</Volume><Issue>4</Issue><PubDate><MedlineDate>2013 Jul-Aug</MedlineDate></PubDate></JournalIssue><Title>Voprosy virusologii</Title><ISOAbbreviation>Vopr. Virusol.</ISOAbbreviation></Journal><ArticleTitle>[Pathogenic effect of pandemic influenza virus H1N1 under replication in cultures of human cells].</ArticleTitle><Pagination><MedlinePgn>20-8</MedlinePgn></Pagination><Abstract><AbstractText>The propagation of the pandemic influenza virus H1N1 in cultures of bronchial (Calu-3) and intestinal (Caco-2) differentiated epithelial cells of human origin was studied. The canine epithelial cell lines, MDCK-H and MDCK-2, were comparatively tested. The two human cell lines were found to be highly sensitive to the influenza pandemic strains A/Hamburg/05/09 and A/Moscow/501/2011 and maintained their replication without addition of trypsin to culture medium. Virus strains of seasonal influenza H1N1, such as A/Moscow/450/2003, A/Memphis/14/96, and laboratory strain A/PR/8/34, multiplied in these human cells in similar manner. The intracellular cleavage HA0-->HA1+HA2 by the host virus-activating protease (IAP) occurred in both human cell lines under infection with each influenza virus H1N1 including pandemic ones. Comparatively, this cleavage of all influenza H1N1 virus strains appeared to be either undetectable or low-detectible in MDCK-H and MDCK-2, respectively, thereby implying low levels of active IAP in these cells. Multiplication of pandemic and seasonal influenza H1N1 viruses in Calu-3 and Caco-2 cells caused cytopathic effect, which was accompanied with low autophagy and apoptosis events. These data allow recommending human cell lines, Calu-3 and Caco-2, for optimized isolation and passaging of clinical strains of Influenza pandemic viruses H1N1.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhirnov</LastName><ForeName>O P</ForeName><Initials>OP</Initials></Author><Author ValidYN="Y"><LastName>Vorob'eva</LastName><ForeName>I V</ForeName><Initials>IV</Initials></Author><Author ValidYN="Y"><LastName>Safonova</LastName><ForeName>O A</ForeName><Initials>OA</Initials></Author><Author ValidYN="Y"><LastName>Malyshev</LastName><ForeName>N A</ForeName><Initials>NA</Initials></Author><Author ValidYN="Y"><LastName>Schwalm</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Klenk</LastName><ForeName>H -D</ForeName><Initials>H-</Initials></Author></AuthorList><Language>rus</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Russia (Federation)</Country><MedlineTA>Vopr Virusol</MedlineTA><NlmUniqueID>0417337</NlmUniqueID><ISSNLinking>0507-4088</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018938" MajorTopicYN="N">Caco-2 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003588" MajorTopicYN="N">Cytopathogenic Effect, Viral</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061985" MajorTopicYN="N">Madin Darby Canine Kidney Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="Y">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>12</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>12</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>1</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24354061</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Klenk, H D" sort="Klenk, H D" uniqKey="Klenk H" first="H D" last="Klenk">H D Klenk</name><name sortKey="Malyshev, N A" sort="Malyshev, N A" uniqKey="Malyshev N" first="N A" last="Malyshev">N A Malyshev</name><name sortKey="Safonova, O A" sort="Safonova, O A" uniqKey="Safonova O" first="O A" last="Safonova">O A Safonova</name><name sortKey="Schwalm, F" sort="Schwalm, F" uniqKey="Schwalm F" first="F" last="Schwalm">F. Schwalm</name><name sortKey="Vorob Eva, I V" sort="Vorob Eva, I V" uniqKey="Vorob Eva I" first="I V" last="Vorob'Eva">I V Vorob'Eva</name><name sortKey="Zhirnov, O P" sort="Zhirnov, O P" uniqKey="Zhirnov O" first="O P" last="Zhirnov">O P Zhirnov</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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