SrasV1, PubMed, Corpus, bibRecord, 000A31

MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.

Identifieur interne : 000A31 ( PubMed/Corpus ); précédent : 000A30; suivant : 000A32

MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.

Auteurs : Vineet D. Menachery ; Alexandra Sch Fer ; Kristin E. Burnum-Johnson ; Hugh D. Mitchell ; Amie J. Eisfeld ; Kevin B. Walters ; Carrie D. Nicora ; Samuel O. Purvine ; Cameron P. Casey ; Matthew E. Monroe ; Karl K. Weitz ; Kelly G. Stratton ; Bobbie-Jo M. Webb-Robertson ; Lisa E. Gralinski ; Thomas O. Metz ; Richard D. Smith ; Katrina M. Waters ; Amy C. Sims ; Yoshihiro Kawaoka ; Ralph S. Baric

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2018.

RBID : pubmed:29339515

English descriptors

KwdEn :
- Animals, Antigen Presentation, Antigenic Variation, Cell Line, Chlorocebus aethiops, DNA Methylation, Dogs, Down-Regulation, Epigenesis, Genetic, Histones (chemistry), Humans, Influenza A Virus, H5N1 Subtype (pathogenicity), Madin Darby Canine Kidney Cells, Major Histocompatibility Complex, Middle East Respiratory Syndrome Coronavirus (pathogenicity), Mutation, Open Reading Frames, Proteomics, Vero Cells.
MESH :
- chemical , chemistry : Histones.
- pathogenicity : Influenza A Virus, H5N1 Subtype, Middle East Respiratory Syndrome Coronavirus.
- Animals, Antigen Presentation, Antigenic Variation, Cell Line, Chlorocebus aethiops, DNA Methylation, Dogs, Down-Regulation, Epigenesis, Genetic, Humans, Madin Darby Canine Kidney Cells, Major Histocompatibility Complex, Mutation, Open Reading Frames, Proteomics, Vero Cells.

Abstract

Convergent evolution dictates that diverse groups of viruses will target both similar and distinct host pathways to manipulate the immune response and improve infection. In this study, we sought to leverage this uneven viral antagonism to identify critical host factors that govern disease outcome. Utilizing a systems-based approach, we examined differential regulation of IFN-γ-dependent genes following infection with robust respiratory viruses including influenza viruses [A/influenza/Vietnam/1203/2004 (H5N1-VN1203) and A/influenza/California/04/2009 (H1N1-CA04)] and coronaviruses [severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV)]. Categorizing by function, we observed down-regulation of gene expression associated with antigen presentation following both H5N1-VN1203 and MERS-CoV infection. Further examination revealed global down-regulation of antigen-presentation gene expression, which was confirmed by proteomics for both H5N1-VN1203 and MERS-CoV infection. Importantly, epigenetic analysis suggested that DNA methylation, rather than histone modification, plays a crucial role in MERS-CoV-mediated antagonism of antigen-presentation gene expression; in contrast, H5N1-VN1203 likely utilizes a combination of epigenetic mechanisms to target antigen presentation. Together, the results indicate a common mechanism utilized by H5N1-VN1203 and MERS-CoV to modulate antigen presentation and the host adaptive immune response.

DOI: 10.1073/pnas.1706928115
PubMed: 29339515

Links to Exploration step

pubmed:29339515

Le document en format XML

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<affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555.</nlm:affiliation>
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<author><name sortKey="Sch Fer, Alexandra" sort="Sch Fer, Alexandra" uniqKey="Sch Fer A" first="Alexandra" last="Sch Fer">Alexandra Sch Fer</name>
<affiliation><nlm:affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.</nlm:affiliation>
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<author><name sortKey="Burnum Johnson, Kristin E" sort="Burnum Johnson, Kristin E" uniqKey="Burnum Johnson K" first="Kristin E" last="Burnum-Johnson">Kristin E. Burnum-Johnson</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.</title>
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<author><name sortKey="Burnum Johnson, Kristin E" sort="Burnum Johnson, Kristin E" uniqKey="Burnum Johnson K" first="Kristin E" last="Burnum-Johnson">Kristin E. Burnum-Johnson</name>
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</affiliation>
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</affiliation>
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</affiliation>
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<author><name sortKey="Purvine, Samuel O" sort="Purvine, Samuel O" uniqKey="Purvine S" first="Samuel O" last="Purvine">Samuel O. Purvine</name>
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</affiliation>
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<author><name sortKey="Casey, Cameron P" sort="Casey, Cameron P" uniqKey="Casey C" first="Cameron P" last="Casey">Cameron P. Casey</name>
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</affiliation>
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<author><name sortKey="Monroe, Matthew E" sort="Monroe, Matthew E" uniqKey="Monroe M" first="Matthew E" last="Monroe">Matthew E. Monroe</name>
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</affiliation>
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<author><name sortKey="Weitz, Karl K" sort="Weitz, Karl K" uniqKey="Weitz K" first="Karl K" last="Weitz">Karl K. Weitz</name>
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</affiliation>
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<author><name sortKey="Stratton, Kelly G" sort="Stratton, Kelly G" uniqKey="Stratton K" first="Kelly G" last="Stratton">Kelly G. Stratton</name>
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<author><name sortKey="Webb Robertson, Bobbie Jo M" sort="Webb Robertson, Bobbie Jo M" uniqKey="Webb Robertson B" first="Bobbie-Jo M" last="Webb-Robertson">Bobbie-Jo M. Webb-Robertson</name>
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</affiliation>
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<author><name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E" last="Gralinski">Lisa E. Gralinski</name>
<affiliation><nlm:affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Sims, Amy C" sort="Sims, Amy C" uniqKey="Sims A" first="Amy C" last="Sims">Amy C. Sims</name>
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</affiliation>
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</affiliation>
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<author><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name>
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</affiliation>
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<term>Antigen Presentation</term>
<term>Antigenic Variation</term>
<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>DNA Methylation</term>
<term>Dogs</term>
<term>Down-Regulation</term>
<term>Epigenesis, Genetic</term>
<term>Histones (chemistry)</term>
<term>Humans</term>
<term>Influenza A Virus, H5N1 Subtype (pathogenicity)</term>
<term>Madin Darby Canine Kidney Cells</term>
<term>Major Histocompatibility Complex</term>
<term>Middle East Respiratory Syndrome Coronavirus (pathogenicity)</term>
<term>Mutation</term>
<term>Open Reading Frames</term>
<term>Proteomics</term>
<term>Vero Cells</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Histones</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H5N1 Subtype</term>
<term>Middle East Respiratory Syndrome Coronavirus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Antigen Presentation</term>
<term>Antigenic Variation</term>
<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>DNA Methylation</term>
<term>Dogs</term>
<term>Down-Regulation</term>
<term>Epigenesis, Genetic</term>
<term>Humans</term>
<term>Madin Darby Canine Kidney Cells</term>
<term>Major Histocompatibility Complex</term>
<term>Mutation</term>
<term>Open Reading Frames</term>
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<front><div type="abstract" xml:lang="en">Convergent evolution dictates that diverse groups of viruses will target both similar and distinct host pathways to manipulate the immune response and improve infection. In this study, we sought to leverage this uneven viral antagonism to identify critical host factors that govern disease outcome. Utilizing a systems-based approach, we examined differential regulation of IFN-γ-dependent genes following infection with robust respiratory viruses including influenza viruses [A/influenza/Vietnam/1203/2004 (H5N1-VN1203) and A/influenza/California/04/2009 (H1N1-CA04)] and coronaviruses [severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV)]. Categorizing by function, we observed down-regulation of gene expression associated with antigen presentation following both H5N1-VN1203 and MERS-CoV infection. Further examination revealed global down-regulation of antigen-presentation gene expression, which was confirmed by proteomics for both H5N1-VN1203 and MERS-CoV infection. Importantly, epigenetic analysis suggested that DNA methylation, rather than histone modification, plays a crucial role in MERS-CoV-mediated antagonism of antigen-presentation gene expression; in contrast, H5N1-VN1203 likely utilizes a combination of epigenetic mechanisms to target antigen presentation. Together, the results indicate a common mechanism utilized by H5N1-VN1203 and MERS-CoV to modulate antigen presentation and the host adaptive immune response.</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>07</Month>
<Day>25</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>115</Volume>
<Issue>5</Issue>
<PubDate><Year>2018</Year>
<Month>01</Month>
<Day>30</Day>
</PubDate>
</JournalIssue>
<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation>
</Journal>
<ArticleTitle>MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.</ArticleTitle>
<Pagination><MedlinePgn>E1012-E1021</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1706928115</ELocationID>
<Abstract><AbstractText>Convergent evolution dictates that diverse groups of viruses will target both similar and distinct host pathways to manipulate the immune response and improve infection. In this study, we sought to leverage this uneven viral antagonism to identify critical host factors that govern disease outcome. Utilizing a systems-based approach, we examined differential regulation of IFN-γ-dependent genes following infection with robust respiratory viruses including influenza viruses [A/influenza/Vietnam/1203/2004 (H5N1-VN1203) and A/influenza/California/04/2009 (H1N1-CA04)] and coronaviruses [severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV)]. Categorizing by function, we observed down-regulation of gene expression associated with antigen presentation following both H5N1-VN1203 and MERS-CoV infection. Further examination revealed global down-regulation of antigen-presentation gene expression, which was confirmed by proteomics for both H5N1-VN1203 and MERS-CoV infection. Importantly, epigenetic analysis suggested that DNA methylation, rather than histone modification, plays a crucial role in MERS-CoV-mediated antagonism of antigen-presentation gene expression; in contrast, H5N1-VN1203 likely utilizes a combination of epigenetic mechanisms to target antigen presentation. Together, the results indicate a common mechanism utilized by H5N1-VN1203 and MERS-CoV to modulate antigen presentation and the host adaptive immune response.</AbstractText>
<CopyrightInformation>Copyright © 2018 the Author(s). Published by PNAS.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Menachery</LastName>
<ForeName>Vineet D</ForeName>
<Initials>VD</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schäfer</LastName>
<ForeName>Alexandra</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Burnum-Johnson</LastName>
<ForeName>Kristin E</ForeName>
<Initials>KE</Initials>
<Identifier Source="ORCID">0000-0002-2722-4149</Identifier>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mitchell</LastName>
<ForeName>Hugh D</ForeName>
<Initials>HD</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eisfeld</LastName>
<ForeName>Amie J</ForeName>
<Initials>AJ</Initials>
<AffiliationInfo><Affiliation>Influenza Research Institute, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Walters</LastName>
<ForeName>Kevin B</ForeName>
<Initials>KB</Initials>
<AffiliationInfo><Affiliation>Influenza Research Institute, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nicora</LastName>
<ForeName>Carrie D</ForeName>
<Initials>CD</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Purvine</LastName>
<ForeName>Samuel O</ForeName>
<Initials>SO</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Casey</LastName>
<ForeName>Cameron P</ForeName>
<Initials>CP</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Monroe</LastName>
<ForeName>Matthew E</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Weitz</LastName>
<ForeName>Karl K</ForeName>
<Initials>KK</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Stratton</LastName>
<ForeName>Kelly G</ForeName>
<Initials>KG</Initials>
<AffiliationInfo><Affiliation>Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99354.</Affiliation>
</AffiliationInfo>
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<CoiStatement>Conflict of interest statement: Y.K. has received speaker’s honoraria from Toyama Chemical and Astellas Inc.; and grant support from Chugai Pharmaceuticals, Daiichi Sankyo Pharmaceutical, Toyama Chemical, Tauns Laboratories, Inc., and Otsuka Pharmaceutical Co., Ltd. Y.K. is a founder of FluGen.</CoiStatement>
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MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.

MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape.

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