Influenza A virus H5N1 entry into host cells is through clathrin-dependent endocytosis.
Identifieur interne : 001778 ( Main/Exploration ); précédent : 001777; suivant : 001779Influenza A virus H5N1 entry into host cells is through clathrin-dependent endocytosis.
Auteurs : Hongliang Wang [République populaire de Chine] ; Chengyu JiangSource :
- Science in China. Series C, Life sciences [ 1006-9305 ] ; 2009.
Descripteurs français
- KwdFr :
- Cavéoles (métabolisme), Chaines lourdes de la clathrine (génétique), Chaines lourdes de la clathrine (métabolisme), Chloroquine (pharmacologie), Clathrine (génétique), Clathrine (métabolisme), Endocytose (), Endocytose (physiologie), Humains, Lignée cellulaire tumorale, Macrolides (pharmacologie), Petit ARN interférent (génétique), Pénétration virale, Sous-type H5N1 du virus de la grippe A (physiologie), Survie cellulaire (), Technique de Western, Transfection.
- MESH :
- génétique : Chaines lourdes de la clathrine, Clathrine, Petit ARN interférent.
- métabolisme : Cavéoles, Chaines lourdes de la clathrine, Clathrine.
- pharmacologie : Chloroquine, Macrolides.
- physiologie : Endocytose, Sous-type H5N1 du virus de la grippe A.
- Endocytose, Humains, Lignée cellulaire tumorale, Pénétration virale, Survie cellulaire, Technique de Western, Transfection.
English descriptors
- KwdEn :
- Blotting, Western, Caveolae (metabolism), Cell Line, Tumor, Cell Survival (drug effects), Chloroquine (pharmacology), Clathrin (genetics), Clathrin (metabolism), Clathrin Heavy Chains (genetics), Clathrin Heavy Chains (metabolism), Endocytosis (drug effects), Endocytosis (physiology), Humans, Influenza A Virus, H5N1 Subtype (physiology), Macrolides (pharmacology), RNA, Small Interfering (genetics), Transfection, Virus Internalization.
- MESH :
- chemical , genetics : Clathrin, Clathrin Heavy Chains, RNA, Small Interfering.
- chemical , metabolism : Clathrin, Clathrin Heavy Chains.
- chemical , pharmacology : Chloroquine, Macrolides.
- drug effects : Cell Survival, Endocytosis.
- metabolism : Caveolae.
- physiology : Endocytosis, Influenza A Virus, H5N1 Subtype.
- Blotting, Western, Cell Line, Tumor, Humans, Transfection, Virus Internalization.
Abstract
Influenza A virus H5N1 presents a major threat to human health. The entry of influenza virus into host cells is believed to be mediated by hemagglutinin (HA), a virus surface glycoprotein that can bind terminal sialic acid residues on host cell glycoproteins and glycolipids. In this study, we elucidated the pathways through which H5N1 enters human lung carcinoma cell line A549. We first proved that H5N1 can enter A549 cells via endocytosis, as lysosomotropic agents, such as bafilomycin A1 and chloroquine, can rescue H5N1-induced A549 cell death. By using specific inhibitors, and siRNAs that target the clathrin pathway, we further found that H5N1 could enter A549 cells via clathrin-mediated endocytosis, while inhibitors targeting caveolae-mediated endocytosis could not inhibit H5N1 cell entry. These findings expand our understanding of H5N1 pathogenesis and provide new information for anti-viral drug research.
DOI: 10.1007/s11427-009-0061-0
PubMed: 19471869
Affiliations:
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Le document en format XML
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<term>Cell Line, Tumor</term>
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<term>Chloroquine (pharmacology)</term>
<term>Clathrin (genetics)</term>
<term>Clathrin (metabolism)</term>
<term>Clathrin Heavy Chains (genetics)</term>
<term>Clathrin Heavy Chains (metabolism)</term>
<term>Endocytosis (drug effects)</term>
<term>Endocytosis (physiology)</term>
<term>Humans</term>
<term>Influenza A Virus, H5N1 Subtype (physiology)</term>
<term>Macrolides (pharmacology)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Transfection</term>
<term>Virus Internalization</term>
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<term>Chaines lourdes de la clathrine (génétique)</term>
<term>Chaines lourdes de la clathrine (métabolisme)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Clathrine (génétique)</term>
<term>Clathrine (métabolisme)</term>
<term>Endocytose ()</term>
<term>Endocytose (physiologie)</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Macrolides (pharmacologie)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Pénétration virale</term>
<term>Sous-type H5N1 du virus de la grippe A (physiologie)</term>
<term>Survie cellulaire ()</term>
<term>Technique de Western</term>
<term>Transfection</term>
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<term>Clathrin Heavy Chains</term>
<term>RNA, Small Interfering</term>
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<term>Clathrin Heavy Chains</term>
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<term>Macrolides</term>
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<term>Clathrine</term>
<term>Petit ARN interférent</term>
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<term>Chaines lourdes de la clathrine</term>
<term>Clathrine</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term>
<term>Macrolides</term>
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<term>Sous-type H5N1 du virus de la grippe A</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Endocytosis</term>
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<term>Transfection</term>
<term>Virus Internalization</term>
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<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Pénétration virale</term>
<term>Survie cellulaire</term>
<term>Technique de Western</term>
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<front><div type="abstract" xml:lang="en">Influenza A virus H5N1 presents a major threat to human health. The entry of influenza virus into host cells is believed to be mediated by hemagglutinin (HA), a virus surface glycoprotein that can bind terminal sialic acid residues on host cell glycoproteins and glycolipids. In this study, we elucidated the pathways through which H5N1 enters human lung carcinoma cell line A549. We first proved that H5N1 can enter A549 cells via endocytosis, as lysosomotropic agents, such as bafilomycin A1 and chloroquine, can rescue H5N1-induced A549 cell death. By using specific inhibitors, and siRNAs that target the clathrin pathway, we further found that H5N1 could enter A549 cells via clathrin-mediated endocytosis, while inhibitors targeting caveolae-mediated endocytosis could not inhibit H5N1 cell entry. These findings expand our understanding of H5N1 pathogenesis and provide new information for anti-viral drug research.</div>
</front>
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