Host regulatory network response to infection with highly pathogenic H5N1 avian influenza virus.
Identifieur interne : 000611 ( PubMed/Corpus ); précédent : 000610; suivant : 000612Host regulatory network response to infection with highly pathogenic H5N1 avian influenza virus.
Auteurs : Chengjun Li ; Armand Bankhead ; Amie J. Eisfeld ; Yasuko Hatta ; Sophia Jeng ; Jean H. Chang ; Lauri D. Aicher ; Sean Proll ; Amy L. Ellis ; G Lynn Law ; Katrina M. Waters ; Gabriele Neumann ; Michael G. Katze ; Shannon Mcweeney ; Yoshihiro KawaokaSource :
- Journal of virology [ 1098-5514 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Cell Line, Epithelial Cells (physiology), Epithelial Cells (virology), Gene Expression Profiling, Gene Expression Regulation, Humans, Influenza A Virus, H5N1 Subtype (immunology), Influenza A Virus, H5N1 Subtype (pathogenicity), Mice, Respiratory Mucosa (cytology), Signal Transduction, Stress, Physiological.
- MESH :
- cytology : Respiratory Mucosa.
- immunology : Influenza A Virus, H5N1 Subtype.
- pathogenicity : Influenza A Virus, H5N1 Subtype.
- physiology : Epithelial Cells.
- virology : Epithelial Cells.
- Animals, Cell Line, Gene Expression Profiling, Gene Expression Regulation, Humans, Mice, Signal Transduction, Stress, Physiological.
Abstract
During the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a system approach to identify and statistically validate signaling subnetworks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). Importantly, we validated a subset of transcripts from one subnetwork in both Calu-3 cells and mice. A more detailed examination of two subnetworks involved in the immune response and keratinization processes revealed potential novel mediators of HPAI H5N1 pathogenesis and host response signaling. Finally, we show how these results compare to those for a less virulent strain of influenza virus. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection and identify novel avenues for perturbation studies and potential therapeutic interventions for fatal HPAI H5N1 disease.
DOI: 10.1128/JVI.05792-11
PubMed: 21865398
Links to Exploration step
pubmed:21865398Le document en format XML
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Eisfeld</name></author><author><name sortKey="Hatta, Yasuko" sort="Hatta, Yasuko" uniqKey="Hatta Y" first="Yasuko" last="Hatta">Yasuko Hatta</name></author><author><name sortKey="Jeng, Sophia" sort="Jeng, Sophia" uniqKey="Jeng S" first="Sophia" last="Jeng">Sophia Jeng</name></author><author><name sortKey="Chang, Jean H" sort="Chang, Jean H" uniqKey="Chang J" first="Jean H" last="Chang">Jean H. Chang</name></author><author><name sortKey="Aicher, Lauri D" sort="Aicher, Lauri D" uniqKey="Aicher L" first="Lauri D" last="Aicher">Lauri D. Aicher</name></author><author><name sortKey="Proll, Sean" sort="Proll, Sean" uniqKey="Proll S" first="Sean" last="Proll">Sean Proll</name></author><author><name sortKey="Ellis, Amy L" sort="Ellis, Amy L" uniqKey="Ellis A" first="Amy L" last="Ellis">Amy L. 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Eisfeld</name></author><author><name sortKey="Hatta, Yasuko" sort="Hatta, Yasuko" uniqKey="Hatta Y" first="Yasuko" last="Hatta">Yasuko Hatta</name></author><author><name sortKey="Jeng, Sophia" sort="Jeng, Sophia" uniqKey="Jeng S" first="Sophia" last="Jeng">Sophia Jeng</name></author><author><name sortKey="Chang, Jean H" sort="Chang, Jean H" uniqKey="Chang J" first="Jean H" last="Chang">Jean H. Chang</name></author><author><name sortKey="Aicher, Lauri D" sort="Aicher, Lauri D" uniqKey="Aicher L" first="Lauri D" last="Aicher">Lauri D. Aicher</name></author><author><name sortKey="Proll, Sean" sort="Proll, Sean" uniqKey="Proll S" first="Sean" last="Proll">Sean Proll</name></author><author><name sortKey="Ellis, Amy L" sort="Ellis, Amy L" uniqKey="Ellis A" first="Amy L" last="Ellis">Amy L. Ellis</name></author><author><name sortKey="Law, G Lynn" sort="Law, G Lynn" uniqKey="Law G" first="G Lynn" last="Law">G Lynn Law</name></author><author><name sortKey="Waters, Katrina M" sort="Waters, Katrina M" uniqKey="Waters K" first="Katrina M" last="Waters">Katrina M. Waters</name></author><author><name sortKey="Neumann, Gabriele" sort="Neumann, Gabriele" uniqKey="Neumann G" first="Gabriele" last="Neumann">Gabriele Neumann</name></author><author><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name></author><author><name sortKey="Mcweeney, Shannon" sort="Mcweeney, Shannon" uniqKey="Mcweeney S" first="Shannon" last="Mcweeney">Shannon Mcweeney</name></author><author><name sortKey="Kawaoka, Yoshihiro" sort="Kawaoka, Yoshihiro" uniqKey="Kawaoka Y" first="Yoshihiro" last="Kawaoka">Yoshihiro Kawaoka</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Epithelial Cells (physiology)</term><term>Epithelial Cells (virology)</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Humans</term><term>Influenza A Virus, H5N1 Subtype (immunology)</term><term>Influenza A Virus, H5N1 Subtype (pathogenicity)</term><term>Mice</term><term>Respiratory Mucosa (cytology)</term><term>Signal Transduction</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A Virus, H5N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H5N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Humans</term><term>Mice</term><term>Signal Transduction</term><term>Stress, Physiological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">During the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a system approach to identify and statistically validate signaling subnetworks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). Importantly, we validated a subset of transcripts from one subnetwork in both Calu-3 cells and mice. A more detailed examination of two subnetworks involved in the immune response and keratinization processes revealed potential novel mediators of HPAI H5N1 pathogenesis and host response signaling. Finally, we show how these results compare to those for a less virulent strain of influenza virus. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection and identify novel avenues for perturbation studies and potential therapeutic interventions for fatal HPAI H5N1 disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21865398</PMID><DateCompleted><Year>2011</Year><Month>11</Month><Day>21</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>85</Volume><Issue>21</Issue><PubDate><Year>2011</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Host regulatory network response to infection with highly pathogenic H5N1 avian influenza virus.</ArticleTitle><Pagination><MedlinePgn>10955-67</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.05792-11</ELocationID><Abstract><AbstractText>During the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a system approach to identify and statistically validate signaling subnetworks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). Importantly, we validated a subset of transcripts from one subnetwork in both Calu-3 cells and mice. A more detailed examination of two subnetworks involved in the immune response and keratinization processes revealed potential novel mediators of HPAI H5N1 pathogenesis and host response signaling. Finally, we show how these results compare to those for a less virulent strain of influenza virus. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection and identify novel avenues for perturbation studies and potential therapeutic interventions for fatal HPAI H5N1 disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Chengjun</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>University of Wisconsin-Madison, School of Veterinary Medicine, Department of Pathobiological Sciences, Influenza Research Institute, 575 Science Drive, Madison, WI 53711, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bankhead</LastName><ForeName>Armand</ForeName><Initials>A</Initials><Suffix>3rd</Suffix></Author><Author ValidYN="Y"><LastName>Eisfeld</LastName><ForeName>Amie J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Hatta</LastName><ForeName>Yasuko</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Jeng</LastName><ForeName>Sophia</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>Jean H</ForeName><Initials>JH</Initials></Author><Author ValidYN="Y"><LastName>Aicher</LastName><ForeName>Lauri D</ForeName><Initials>LD</Initials></Author><Author ValidYN="Y"><LastName>Proll</LastName><ForeName>Sean</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ellis</LastName><ForeName>Amy L</ForeName><Initials>AL</Initials></Author><Author ValidYN="Y"><LastName>Law</LastName><ForeName>G Lynn</ForeName><Initials>GL</Initials></Author><Author ValidYN="Y"><LastName>Waters</LastName><ForeName>Katrina M</ForeName><Initials>KM</Initials></Author><Author ValidYN="Y"><LastName>Neumann</LastName><ForeName>Gabriele</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Katze</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>McWeeney</LastName><ForeName>Shannon</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kawaoka</LastName><ForeName>Yoshihiro</ForeName><Initials>Y</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272200800060C</GrantID><Acronym>AO</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 RR024140</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>08</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053124" MajorTopicYN="N">Influenza A 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|area= StressCovidV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:21865398
|texte= Host regulatory network response to infection with highly pathogenic H5N1 avian influenza virus.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:21865398" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a StressCovidV1
| This area was generated with Dilib version V0.6.33. |  |