Inhibition of SARS pseudovirus cell entry by lactoferrin binding to heparan sulfate proteoglycans.
Identifieur interne : 001478 ( PubMed/Curation ); précédent : 001477; suivant : 001479Inhibition of SARS pseudovirus cell entry by lactoferrin binding to heparan sulfate proteoglycans.
Auteurs : Jianshe Lang [République populaire de Chine] ; Ning Yang ; Jiejie Deng ; Kangtai Liu ; Peng Yang ; Guigen Zhang ; Chengyu JiangSource :
- PloS one [ 1932-6203 ] ; 2011.
Descripteurs français
- KwdFr :
- Humains, Lactoferrine (immunologie), Lactoferrine (métabolisme), Lactoferrine (pharmacologie), Liaison aux protéines (immunologie), Lignée cellulaire, Protéoglycanes à sulfate d'héparane (métabolisme), Pénétration virale (), Relation dose-effet des médicaments, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (étiologie), Virus du SRAS (physiologie).
- MESH :
- immunologie : Lactoferrine, Liaison aux protéines, Syndrome respiratoire aigu sévère.
- métabolisme : Lactoferrine, Protéoglycanes à sulfate d'héparane.
- pharmacologie : Lactoferrine.
- physiologie : Virus du SRAS.
- étiologie : Syndrome respiratoire aigu sévère.
- Humains, Lignée cellulaire, Pénétration virale, Relation dose-effet des médicaments, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Cell Line, Dose-Response Relationship, Drug, Heparan Sulfate Proteoglycans (metabolism), Humans, Lactoferrin (immunology), Lactoferrin (metabolism), Lactoferrin (pharmacology), Protein Binding (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (etiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (prevention & control), Virus Internalization (drug effects).
- MESH :
- chemical , immunology : Lactoferrin.
- chemical , metabolism : Heparan Sulfate Proteoglycans, Lactoferrin.
- chemical , pharmacology : Lactoferrin.
- drug effects : Virus Internalization.
- etiology : Severe Acute Respiratory Syndrome.
- immunology : Protein Binding, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- prevention & control : Severe Acute Respiratory Syndrome.
- Cell Line, Dose-Response Relationship, Drug, Humans.
Abstract
It has been reported that lactoferrin (LF) participates in the host immune response against Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) invasion by enhancing NK cell activity and stimulating neutrophil aggregation and adhesion. We further investigated the role of LF in the entry of SARS pseudovirus into HEK293E/ACE2-Myc cells. Our results reveal that LF inhibits SARS pseudovirus infection in a dose-dependent manner. Further analysis suggested that LF was able to block the binding of spike protein to host cells at 4°C, indicating that LF exerted its inhibitory function at the viral attachment stage. However, LF did not disrupt the interaction of spike protein with angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV. Previous studies have shown that LF colocalizes with the widely distributed cell-surface heparan sulfate proteoglycans (HSPGs). Our experiments have also confirmed this conclusion. Treatment of the cells with heparinase or exogenous heparin prevented binding of spike protein to host cells and inhibited SARS pseudovirus infection, demonstrating that HSPGs provide the binding sites for SARS-CoV invasion at the early attachment phase. Taken together, our results suggest that, in addition to ACE2, HSPGs are essential cell-surface molecules involved in SARS-CoV cell entry. LF may play a protective role in host defense against SARS-CoV infection through binding to HSPGs and blocking the preliminary interaction between SARS-CoV and host cells. Our findings may provide further understanding of SARS-CoV pathogenesis and aid in treatment of this deadly disease.
DOI: 10.1371/journal.pone.0023710
PubMed: 21887302
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à sulfate d'héparane (métabolisme)</term><term>Pénétration virale ()</term><term>Relation dose-effet des médicaments</term><term>Syndrome respiratoire aigu sévère ()</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (étiologie)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Lactoferrin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Heparan Sulfate Proteoglycans</term><term>Lactoferrin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Lactoferrin</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Virus Internalization</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunologie" 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We further investigated the role of LF in the entry of SARS pseudovirus into HEK293E/ACE2-Myc cells. Our results reveal that LF inhibits SARS pseudovirus infection in a dose-dependent manner. Further analysis suggested that LF was able to block the binding of spike protein to host cells at 4°C, indicating that LF exerted its inhibitory function at the viral attachment stage. However, LF did not disrupt the interaction of spike protein with angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV. Previous studies have shown that LF colocalizes with the widely distributed cell-surface heparan sulfate proteoglycans (HSPGs). Our experiments have also confirmed this conclusion. Treatment of the cells with heparinase or exogenous heparin prevented binding of spike protein to host cells and inhibited SARS pseudovirus infection, demonstrating that HSPGs provide the binding sites for SARS-CoV invasion at the early attachment phase. Taken together, our results suggest that, in addition to ACE2, HSPGs are essential cell-surface molecules involved in SARS-CoV cell entry. LF may play a protective role in host defense against SARS-CoV infection through binding to HSPGs and blocking the preliminary interaction between SARS-CoV and host cells. Our findings may provide further understanding of SARS-CoV pathogenesis and aid in treatment of this deadly disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21887302</PMID><DateCompleted><Year>2012</Year><Month>02</Month><Day>24</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>8</Issue><PubDate><Year>2011</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Inhibition of SARS pseudovirus cell entry by lactoferrin binding to heparan sulfate proteoglycans.</ArticleTitle><Pagination><MedlinePgn>e23710</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0023710</ELocationID><Abstract><AbstractText>It has been reported that lactoferrin (LF) participates in the host immune response against Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) invasion by enhancing NK cell activity and stimulating neutrophil aggregation and adhesion. We further investigated the role of LF in the entry of SARS pseudovirus into HEK293E/ACE2-Myc cells. Our results reveal that LF inhibits SARS pseudovirus infection in a dose-dependent manner. Further analysis suggested that LF was able to block the binding of spike protein to host cells at 4°C, indicating that LF exerted its inhibitory function at the viral attachment stage. However, LF did not disrupt the interaction of spike protein with angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV. Previous studies have shown that LF colocalizes with the widely distributed cell-surface heparan sulfate proteoglycans (HSPGs). Our experiments have also confirmed this conclusion. Treatment of the cells with heparinase or exogenous heparin prevented binding of spike protein to host cells and inhibited SARS pseudovirus infection, demonstrating that HSPGs provide the binding sites for SARS-CoV invasion at the early attachment phase. Taken together, our results suggest that, in addition to ACE2, HSPGs are essential cell-surface molecules involved in SARS-CoV cell entry. LF may play a protective role in host defense against SARS-CoV infection through binding to HSPGs and blocking the preliminary interaction between SARS-CoV and host cells. Our findings may provide further understanding of SARS-CoV pathogenesis and aid in treatment of this deadly disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Jianshe</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Tsinghua University, Beijing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ning</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Jiejie</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Kangtai</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Peng</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Guigen</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Chengyu</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>08</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019812">Heparan Sulfate Proteoglycans</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber><NameOfSubstance 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