Lipid rafts play an important role in the early stage of severe acute respiratory syndrome-coronavirus life cycle.
Identifieur interne : 001823 ( Ncbi/Curation ); précédent : 001822; suivant : 001824Lipid rafts play an important role in the early stage of severe acute respiratory syndrome-coronavirus life cycle.
Auteurs : Gui-Mei Li [Japon] ; Yong-Gang Li ; Masanobu Yamate ; Shu-Ming Li ; Kazuyoshi IkutaSource :
- Microbes and infection [ 1286-4579 ] ; 2007.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux, Cellules Vero, Cholestérol (déficit), Cholestérol (métabolisme), Cholestérol (pharmacologie), Cyclodextrines bêta (pharmacologie), Cytométrie en flux, Microdomaines membranaires (métabolisme), Microdomaines membranaires (virologie), Peptidyl-Dipeptidase A (métabolisme), Réplication virale (), Réplication virale (physiologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (croissance et développement), Virus du SRAS (génétique), Virus du SRAS (physiologie), Étapes du cycle de vie.
- MESH :
- croissance et développement : Virus du SRAS.
- déficit : Cholestérol.
- génétique : ARN messager, Virus du SRAS.
- métabolisme : ARN messager, Cholestérol, Microdomaines membranaires, Peptidyl-Dipeptidase A, Syndrome respiratoire aigu sévère.
- pharmacologie : Cholestérol, Cyclodextrines bêta.
- physiologie : Réplication virale, Virus du SRAS.
- virologie : Microdomaines membranaires, Syndrome respiratoire aigu sévère.
- Animaux, Cellules Vero, Cytométrie en flux, Réplication virale, Étapes du cycle de vie.
English descriptors
- KwdEn :
- Animals, Chlorocebus aethiops, Cholesterol (deficiency), Cholesterol (metabolism), Cholesterol (pharmacology), Flow Cytometry, Life Cycle Stages, Membrane Microdomains (metabolism), Membrane Microdomains (virology), Peptidyl-Dipeptidase A (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), SARS Virus (genetics), SARS Virus (growth & development), SARS Virus (physiology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Vero Cells, Virus Replication (drug effects), Virus Replication (physiology), beta-Cyclodextrins (pharmacology).
- MESH :
- chemical , deficiency : Cholesterol.
- chemical , genetics : RNA, Messenger.
- chemical , metabolism : Cholesterol, Peptidyl-Dipeptidase A, RNA, Messenger.
- chemical , pharmacology : Cholesterol, beta-Cyclodextrins.
- drug effects : Virus Replication.
- genetics : SARS Virus.
- growth & development : SARS Virus.
- metabolism : Membrane Microdomains, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus, Virus Replication.
- virology : Membrane Microdomains, Severe Acute Respiratory Syndrome.
- Animals, Chlorocebus aethiops, Flow Cytometry, Life Cycle Stages, Vero Cells.
Abstract
Lipid rafts are involved in the life cycle of many viruses. In this study, we showed that lipid rafts also play an important role in the life cycle of severe acute respiratory syndrome (SARS)-coronavirus (CoV). Cholesterol depletion by pretreatment of Vero E6 cells with methyl-beta-cyclodextrin (MbetaCD) inhibited the production of SARS-CoV particles released from the infected cells. This inhibition was prevented by addition of cholesterol to the culture medium, indicating that the reduction of virus particle release was caused by the loss of cholesterol in the cell membrane. In contrast, cholesterol depletion at the post-entry stage (3h post-infection) caused only a limited effect on virus particle release. Northern blot analysis revealed that the levels of viral mRNAs were significantly affected by pretreatment with MbetaCD, but not by treatment at 3h post-infection. Interestingly, no apparent evidence for colocalization of angiotensin converting enzyme 2 with lipid rafts in the membrane of Vero E6 cells was obtained. These results suggest that lipid rafts could contribute to SARS-CoV infection in the early replication process in Vero E6 cells.
DOI: 10.1016/j.micinf.2006.10.015
PubMed: 17194611
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pubmed:17194611Le document en format XML
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<author><name sortKey="Li, Gui Mei" sort="Li, Gui Mei" uniqKey="Li G" first="Gui-Mei" last="Li">Gui-Mei Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Virology, Research Institute for Microbial Diseases (RIMD), Osaka University, Suita, Osaka 565-0871, Japan.</nlm:affiliation>
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<author><name sortKey="Yamate, Masanobu" sort="Yamate, Masanobu" uniqKey="Yamate M" first="Masanobu" last="Yamate">Masanobu Yamate</name>
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<term>Cholesterol (pharmacology)</term>
<term>Flow Cytometry</term>
<term>Life Cycle Stages</term>
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<term>Membrane Microdomains (virology)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
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<term>Cholestérol (métabolisme)</term>
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<term>Life Cycle Stages</term>
<term>Vero Cells</term>
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<front><div type="abstract" xml:lang="en">Lipid rafts are involved in the life cycle of many viruses. In this study, we showed that lipid rafts also play an important role in the life cycle of severe acute respiratory syndrome (SARS)-coronavirus (CoV). Cholesterol depletion by pretreatment of Vero E6 cells with methyl-beta-cyclodextrin (MbetaCD) inhibited the production of SARS-CoV particles released from the infected cells. This inhibition was prevented by addition of cholesterol to the culture medium, indicating that the reduction of virus particle release was caused by the loss of cholesterol in the cell membrane. In contrast, cholesterol depletion at the post-entry stage (3h post-infection) caused only a limited effect on virus particle release. Northern blot analysis revealed that the levels of viral mRNAs were significantly affected by pretreatment with MbetaCD, but not by treatment at 3h post-infection. Interestingly, no apparent evidence for colocalization of angiotensin converting enzyme 2 with lipid rafts in the membrane of Vero E6 cells was obtained. These results suggest that lipid rafts could contribute to SARS-CoV infection in the early replication process in Vero E6 cells.</div>
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