Host cell kinases and the hepatitis C virus life cycle.
Identifieur interne : 002485 ( Ncbi/Merge ); précédent : 002484; suivant : 002486Host cell kinases and the hepatitis C virus life cycle.
Auteurs : Che C. Colpitts [France] ; Joachim Lupberger [France] ; Christian Doerig [Australie] ; Thomas F. Baumert [France]Source :
- Biochimica et biophysica acta [ 0006-3002 ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Antigènes mineurs d'histocompatibilité, Assemblage viral (génétique), Hepacivirus (génétique), Hepacivirus (pathogénicité), Humains, Hépatite C (génétique), Hépatite C (virologie), Hépatocytes (enzymologie), Hépatocytes (virologie), Interactions hôte-pathogène (génétique), Phosphotransferases (Alcohol Group Acceptor) (génétique), Protéines virales non structurales (génétique), Pénétration virale, Récepteur EphA2 (génétique), Récepteur du facteur de croissance épidermique (génétique), Récepteur du facteur de croissance épidermique (métabolisme), Étapes du cycle de vie (génétique).
- MESH :
- enzymologie : Hépatocytes.
- génétique : Assemblage viral, Hepacivirus, Hépatite C, Interactions hôte-pathogène, Phosphotransferases (Alcohol Group Acceptor), Protéines virales non structurales, Récepteur EphA2, Récepteur du facteur de croissance épidermique, Étapes du cycle de vie.
- métabolisme : Récepteur du facteur de croissance épidermique.
- pathogénicité : Hepacivirus.
- virologie : Hépatite C, Hépatocytes.
- Animaux, Antigènes mineurs d'histocompatibilité, Humains, Pénétration virale.
English descriptors
- KwdEn :
- Animals, Hepacivirus (genetics), Hepacivirus (pathogenicity), Hepatitis C (genetics), Hepatitis C (virology), Hepatocytes (enzymology), Hepatocytes (virology), Host-Pathogen Interactions (genetics), Humans, Life Cycle Stages (genetics), Minor Histocompatibility Antigens, Phosphotransferases (Alcohol Group Acceptor) (genetics), Receptor, EphA2 (genetics), Receptor, Epidermal Growth Factor (genetics), Receptor, Epidermal Growth Factor (metabolism), Viral Nonstructural Proteins (genetics), Virus Assembly (genetics), Virus Internalization.
- MESH :
- chemical , genetics : Phosphotransferases (Alcohol Group Acceptor), Receptor, EphA2, Receptor, Epidermal Growth Factor, Viral Nonstructural Proteins.
- chemical , metabolism : Receptor, Epidermal Growth Factor.
- chemical : Minor Histocompatibility Antigens.
- enzymology : Hepatocytes.
- genetics : Hepacivirus, Hepatitis C, Host-Pathogen Interactions, Life Cycle Stages, Virus Assembly.
- pathogenicity : Hepacivirus.
- virology : Hepatitis C, Hepatocytes.
- Animals, Humans, Virus Internalization.
Abstract
Hepatitis C virus (HCV) infection relies on virus-host interactions with human hepatocytes, a context in which host cell kinases play critical roles in every step of the HCV life cycle. During viral entry, cellular kinases, including EGFR, EphA2 and PKA, regulate the localization of host HCV entry factors and induce receptor complex assembly. Following virion internalization, viral genomes replicate on endoplasmic reticulum-derived membranous webs. The formation of membranous webs depends on interactions between the HCV NS5a protein and PI4KIIIα. The phosphorylation status of NS5a, regulated by PI4KIIIα, CKI and other kinases, also acts as a molecular switch to virion assembly, which takes place on lipid droplets. The formation of lipid droplets is enhanced by HCV activation of IKKα. In view of the multiple crucial steps in the viral life cycle that are mediated by host cell kinases, these enzymes also represent complementary targets for antiviral therapy. This article is part of a Special Issue entitled: Inhibitors of Protein Kinases.
DOI: 10.1016/j.bbapap.2015.04.011
PubMed: 25896387
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xml:lang="en"><term>Animals</term><term>Hepacivirus (genetics)</term><term>Hepacivirus (pathogenicity)</term><term>Hepatitis C (genetics)</term><term>Hepatitis C (virology)</term><term>Hepatocytes (enzymology)</term><term>Hepatocytes (virology)</term><term>Host-Pathogen Interactions (genetics)</term><term>Humans</term><term>Life Cycle Stages (genetics)</term><term>Minor Histocompatibility Antigens</term><term>Phosphotransferases (Alcohol Group Acceptor) (genetics)</term><term>Receptor, EphA2 (genetics)</term><term>Receptor, Epidermal Growth Factor (genetics)</term><term>Receptor, Epidermal Growth Factor (metabolism)</term><term>Viral Nonstructural Proteins (genetics)</term><term>Virus Assembly (genetics)</term><term>Virus Internalization</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigènes mineurs d'histocompatibilité</term><term>Assemblage viral (génétique)</term><term>Hepacivirus (génétique)</term><term>Hepacivirus (pathogénicité)</term><term>Humains</term><term>Hépatite C (génétique)</term><term>Hépatite C (virologie)</term><term>Hépatocytes (enzymologie)</term><term>Hépatocytes (virologie)</term><term>Interactions hôte-pathogène (génétique)</term><term>Phosphotransferases (Alcohol Group Acceptor) (génétique)</term><term>Protéines virales non structurales (génétique)</term><term>Pénétration virale</term><term>Récepteur EphA2 (génétique)</term><term>Récepteur du facteur de croissance épidermique (génétique)</term><term>Récepteur du facteur de croissance épidermique (métabolisme)</term><term>Étapes du cycle de vie (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Receptor, EphA2</term><term>Receptor, Epidermal Growth Factor</term><term>Viral Nonstructural Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptor, Epidermal Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Minor Histocompatibility Antigens</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Hépatocytes</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Hepatocytes</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hepacivirus</term><term>Hepatitis C</term><term>Host-Pathogen Interactions</term><term>Life Cycle Stages</term><term>Virus Assembly</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Assemblage viral</term><term>Hepacivirus</term><term>Hépatite C</term><term>Interactions hôte-pathogène</term><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Protéines virales non structurales</term><term>Récepteur EphA2</term><term>Récepteur du facteur de croissance épidermique</term><term>Étapes du cycle de vie</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Récepteur du facteur de croissance épidermique</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Hepacivirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Hepacivirus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Hépatite C</term><term>Hépatocytes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Hepatitis C</term><term>Hepatocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Virus Internalization</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antigènes mineurs d'histocompatibilité</term><term>Humains</term><term>Pénétration virale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hepatitis C virus (HCV) infection relies on virus-host interactions with human hepatocytes, a context in which host cell kinases play critical roles in every step of the HCV life cycle. During viral entry, cellular kinases, including EGFR, EphA2 and PKA, regulate the localization of host HCV entry factors and induce receptor complex assembly. Following virion internalization, viral genomes replicate on endoplasmic reticulum-derived membranous webs. The formation of membranous webs depends on interactions between the HCV NS5a protein and PI4KIIIα. The phosphorylation status of NS5a, regulated by PI4KIIIα, CKI and other kinases, also acts as a molecular switch to virion assembly, which takes place on lipid droplets. The formation of lipid droplets is enhanced by HCV activation of IKKα. In view of the multiple crucial steps in the viral life cycle that are mediated by host cell kinases, these enzymes also represent complementary targets for antiviral therapy. This article is part of a Special Issue entitled: Inhibitors of Protein Kinases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25896387</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>21</Day></DateCreated><DateCompleted><Year>2015</Year><Month>12</Month><Day>09</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>1854</Volume><Issue>10 Pt B</Issue><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Biochimica et biophysica acta</Title><ISOAbbreviation>Biochim. Biophys. Acta</ISOAbbreviation></Journal><ArticleTitle>Host cell kinases and the hepatitis C virus life cycle.</ArticleTitle><Pagination><MedlinePgn>1657-62</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbapap.2015.04.011</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1570-9639(15)00108-9</ELocationID><Abstract><AbstractText>Hepatitis C virus (HCV) infection relies on virus-host interactions with human hepatocytes, a context in which host cell kinases play critical roles in every step of the HCV life cycle. During viral entry, cellular kinases, including EGFR, EphA2 and PKA, regulate the localization of host HCV entry factors and induce receptor complex assembly. Following virion internalization, viral genomes replicate on endoplasmic reticulum-derived membranous webs. The formation of membranous webs depends on interactions between the HCV NS5a protein and PI4KIIIα. The phosphorylation status of NS5a, regulated by PI4KIIIα, CKI and other kinases, also acts as a molecular switch to virion assembly, which takes place on lipid droplets. The formation of lipid droplets is enhanced by HCV activation of IKKα. In view of the multiple crucial steps in the viral life cycle that are mediated by host cell kinases, these enzymes also represent complementary targets for antiviral therapy. This article is part of a Special Issue entitled: Inhibitors of Protein Kinases.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Colpitts</LastName><ForeName>Che C</ForeName><Initials>CC</Initials><AffiliationInfo><Affiliation>Inserm U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Strasbourg, France; Université de Strasbourg, Strasbourg, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lupberger</LastName><ForeName>Joachim</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Inserm U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Strasbourg, France; Université de Strasbourg, Strasbourg, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Doerig</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Microbiology, School of Biomedical Sciences, Monash University, Victoria, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baumert</LastName><ForeName>Thomas F</ForeName><Initials>TF</Initials><AffiliationInfo><Affiliation>Inserm U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Strasbourg, France; Université de Strasbourg, Strasbourg, France; Institut Hospitalo-Universitaire, Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. Electronic address: thomas.baumert@unistra.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>04</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta</MedlineTA><NlmUniqueID>0217513</NlmUniqueID><ISSNLinking>0006-3002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015778">Minor Histocompatibility Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C087036">NS-5 protein, hepatitis C virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017361">Viral Nonstructural Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D017853">Phosphotransferases (Alcohol Group Acceptor)</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.67</RegistryNumber><NameOfSubstance UI="C402182">phosphatidylinositol phosphate 4-kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C512478">EGFR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D036104">Receptor, EphA2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D011958">Receptor, Epidermal Growth Factor</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016174" MajorTopicYN="N">Hepacivirus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006526" MajorTopicYN="N">Hepatitis C</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022781" MajorTopicYN="N">Hepatocytes</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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Colpitts</name></region><name sortKey="Baumert, Thomas F" sort="Baumert, Thomas F" uniqKey="Baumert T" first="Thomas F" last="Baumert">Thomas F. Baumert</name><name sortKey="Lupberger, Joachim" sort="Lupberger, Joachim" uniqKey="Lupberger J" first="Joachim" last="Lupberger">Joachim Lupberger</name></country><country name="Australie"><noRegion><name sortKey="Doerig, Christian" sort="Doerig, Christian" uniqKey="Doerig C" first="Christian" last="Doerig">Christian Doerig</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Host cell kinases and the hepatitis C virus life cycle.
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