Global impact of influenza virus on cellular pathways is mediated by both replication-dependent and -independent events.
Identifieur interne : 002C86 ( Main/Exploration ); précédent : 002C85; suivant : 002C87Global impact of influenza virus on cellular pathways is mediated by both replication-dependent and -independent events.
Auteurs : G K Geiss [États-Unis] ; M C An ; R E Bumgarner ; E. Hammersmark ; D. Cunningham ; M G KatzeSource :
- Journal of virology [ 0022-538X ] ; 2001.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Orthomyxoviridae.
- physiologie : Orthomyxoviridae.
- Analyse de profil d'expression de gènes, Cellules HeLa, Humains, Rayons ultraviolets, Réplication virale, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- MESH :
- metabolism : Orthomyxoviridae.
- physiology : Orthomyxoviridae.
- Gene Expression Profiling, HeLa Cells, Humans, Oligonucleotide Array Sequence Analysis, Ultraviolet Rays, Virus Replication.
Abstract
Influenza virus, the causative agent of the common flu, is a worldwide health problem with significant economic consequences. Studies of influenza virus biology have revealed elaborate mechanisms by which the virus interacts with its host cell as it inhibits the synthesis of cellular proteins, evades the innate antiviral response, and facilitates production of viral RNAs and proteins. With the advent of DNA array technology it is now possible to obtain a large-scale view of how viruses alter the environment within the host cell. In this study, the cellular response to influenza virus infection was examined by monitoring the steady-state mRNA levels for over 4,600 cellular genes. Infections with active and inactivated influenza viruses identified changes in cellular gene expression that were dependent on or independent of viral replication, respectively. Viral replication resulted in the downregulation of many cellular mRNAs, and the effect was enhanced with time postinfection. Interestingly, several genes involved in protein synthesis, transcriptional regulation, and cytokine signaling were induced by influenza virus replication, suggesting that some may play essential or accessory roles in the viral life cycle or the host cell's stress response. The gene expression pattern induced by inactivated viruses revealed induction of the cellular metallothionein genes that may represent a protective response to virus-induced oxidative stress. Genome-scale analyses of virus infections will help us to understand the complexities of virus-host interactions and may lead to the discovery of novel drug targets or antiviral therapies.
DOI: 10.1128/JVI.75.9.4321-4331.2001
PubMed: 11287581
Affiliations:
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Hammersmark</name></author><author><name sortKey="Cunningham, D" sort="Cunningham, D" uniqKey="Cunningham D" first="D" last="Cunningham">D. Cunningham</name></author><author><name sortKey="Katze, M G" sort="Katze, M G" uniqKey="Katze M" first="M G" last="Katze">M G Katze</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Gene Expression Profiling</term><term>HeLa Cells</term><term>Humans</term><term>Oligonucleotide Array Sequence Analysis</term><term>Orthomyxoviridae (metabolism)</term><term>Orthomyxoviridae (physiology)</term><term>Ultraviolet Rays</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules HeLa</term><term>Humains</term><term>Orthomyxoviridae (métabolisme)</term><term>Orthomyxoviridae (physiologie)</term><term>Rayons ultraviolets</term><term>Réplication virale</term><term>Séquençage par oligonucléotides en batterie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Orthomyxoviridae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Orthomyxoviridae</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Orthomyxoviridae</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Orthomyxoviridae</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Profiling</term><term>HeLa Cells</term><term>Humans</term><term>Oligonucleotide Array Sequence Analysis</term><term>Ultraviolet Rays</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules HeLa</term><term>Humains</term><term>Rayons ultraviolets</term><term>Réplication virale</term><term>Séquençage par oligonucléotides en batterie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza virus, the causative agent of the common flu, is a worldwide health problem with significant economic consequences. Studies of influenza virus biology have revealed elaborate mechanisms by which the virus interacts with its host cell as it inhibits the synthesis of cellular proteins, evades the innate antiviral response, and facilitates production of viral RNAs and proteins. With the advent of DNA array technology it is now possible to obtain a large-scale view of how viruses alter the environment within the host cell. In this study, the cellular response to influenza virus infection was examined by monitoring the steady-state mRNA levels for over 4,600 cellular genes. Infections with active and inactivated influenza viruses identified changes in cellular gene expression that were dependent on or independent of viral replication, respectively. Viral replication resulted in the downregulation of many cellular mRNAs, and the effect was enhanced with time postinfection. Interestingly, several genes involved in protein synthesis, transcriptional regulation, and cytokine signaling were induced by influenza virus replication, suggesting that some may play essential or accessory roles in the viral life cycle or the host cell's stress response. The gene expression pattern induced by inactivated viruses revealed induction of the cellular metallothionein genes that may represent a protective response to virus-induced oxidative stress. Genome-scale analyses of virus infections will help us to understand the complexities of virus-host interactions and may lead to the discovery of novel drug targets or antiviral therapies.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="An, M C" sort="An, M C" uniqKey="An M" first="M C" last="An">M C An</name><name sortKey="Bumgarner, R E" sort="Bumgarner, R E" uniqKey="Bumgarner R" first="R E" last="Bumgarner">R E Bumgarner</name><name sortKey="Cunningham, D" sort="Cunningham, D" uniqKey="Cunningham D" first="D" last="Cunningham">D. Cunningham</name><name sortKey="Hammersmark, E" sort="Hammersmark, E" uniqKey="Hammersmark E" first="E" last="Hammersmark">E. Hammersmark</name><name sortKey="Katze, M G" sort="Katze, M G" uniqKey="Katze M" first="M G" last="Katze">M G Katze</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Geiss, G K" sort="Geiss, G K" uniqKey="Geiss G" first="G K" last="Geiss">G K Geiss</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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