Chinese hamster ovary cell lines selected for resistance to ebolavirus glycoprotein mediated infection are defective for NPC1 expression.
Identifieur interne : 001344 ( PubMed/Corpus ); précédent : 001343; suivant : 001345Chinese hamster ovary cell lines selected for resistance to ebolavirus glycoprotein mediated infection are defective for NPC1 expression.
Auteurs : Kathleen M. Haines ; Nathan H. Vande Burgt ; Joseph R. Francica ; Rachel L. Kaletsky ; Paul BatesSource :
- Virology [ 1096-0341 ] ; 2012.
English descriptors
- KwdEn :
- Animals, CHO Cells, Cricetinae, Cricetulus, Ebolavirus (pathogenicity), Ebolavirus (physiology), Genetic Complementation Test, Host-Pathogen Interactions, Membrane Glycoproteins (biosynthesis), Membrane Glycoproteins (deficiency), Mutation, Receptors, Virus (biosynthesis), Receptors, Virus (deficiency), Virus Internalization.
- MESH :
- chemical , biosynthesis : Membrane Glycoproteins, Receptors, Virus.
- chemical , deficiency : Membrane Glycoproteins, Receptors, Virus.
- pathogenicity : Ebolavirus.
- physiology : Ebolavirus.
- Animals, CHO Cells, Cricetinae, Cricetulus, Genetic Complementation Test, Host-Pathogen Interactions, Mutation, Virus Internalization.
Abstract
Ebolavirus causes severe hemorrhagic fever in humans and non-human primates. Entry of ebolavirus is mediated by the viral glycoprotein, GP; however, the required host factors have not been fully elucidated. A screen utilizing a recombinant Vesicular Stomatitis Virus (VSV) encoding Zaire ebolavirus GP identified four Chinese Hamster Ovary (CHO) cell lines resistant to GP-mediated viral entry. Susceptibility to vectors carrying SARS coronavirus S or VSV-G glycoproteins suggests that endocytic and processing pathways utilized by other viruses are intact in these cells. A cathepsin-activated form of the ebolaviral glycoprotein did not overcome the entry restriction, nor did expression of several host factors previously described as important for ebolavirus entry. Conversely, expression of the recently described ebolavirus host entry factor Niemann-Pick Type C1 (NPC1) restored infection. Resistant cells encode distinct mutations in the NPC1 gene, resulting in loss of protein expression. These studies reinforce the importance of NPC1 for ebolavirus entry.
DOI: 10.1016/j.virol.2012.05.018
PubMed: 22726751
Links to Exploration step
pubmed:22726751Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chinese hamster ovary cell lines selected for resistance to ebolavirus glycoprotein mediated infection are defective for NPC1 expression.</title><author><name sortKey="Haines, Kathleen M" sort="Haines, Kathleen M" uniqKey="Haines K" first="Kathleen M" last="Haines">Kathleen M. Haines</name><affiliation><nlm:affiliation>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6076, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Vande Burgt, Nathan H" sort="Vande Burgt, Nathan H" uniqKey="Vande Burgt N" first="Nathan H" last="Vande Burgt">Nathan H. Vande Burgt</name></author><author><name sortKey="Francica, Joseph R" sort="Francica, Joseph R" uniqKey="Francica J" first="Joseph R" last="Francica">Joseph R. Francica</name></author><author><name sortKey="Kaletsky, Rachel L" sort="Kaletsky, Rachel L" uniqKey="Kaletsky R" first="Rachel L" last="Kaletsky">Rachel L. Kaletsky</name></author><author><name sortKey="Bates, Paul" sort="Bates, Paul" uniqKey="Bates P" first="Paul" last="Bates">Paul Bates</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22726751</idno><idno type="pmid">22726751</idno><idno type="doi">10.1016/j.virol.2012.05.018</idno><idno type="wicri:Area/PubMed/Corpus">001344</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001344</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chinese hamster ovary cell lines selected for resistance to ebolavirus glycoprotein mediated infection are defective for NPC1 expression.</title><author><name sortKey="Haines, Kathleen M" sort="Haines, Kathleen M" uniqKey="Haines K" first="Kathleen M" last="Haines">Kathleen M. Haines</name><affiliation><nlm:affiliation>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6076, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Vande Burgt, Nathan H" sort="Vande Burgt, Nathan H" uniqKey="Vande Burgt N" first="Nathan H" last="Vande Burgt">Nathan H. Vande Burgt</name></author><author><name sortKey="Francica, Joseph R" sort="Francica, Joseph R" uniqKey="Francica J" first="Joseph R" last="Francica">Joseph R. Francica</name></author><author><name sortKey="Kaletsky, Rachel L" sort="Kaletsky, Rachel L" uniqKey="Kaletsky R" first="Rachel L" last="Kaletsky">Rachel L. Kaletsky</name></author><author><name sortKey="Bates, Paul" sort="Bates, Paul" uniqKey="Bates P" first="Paul" last="Bates">Paul Bates</name></author></analytic><series><title level="j">Virology</title><idno type="eISSN">1096-0341</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>CHO Cells</term><term>Cricetinae</term><term>Cricetulus</term><term>Ebolavirus (pathogenicity)</term><term>Ebolavirus (physiology)</term><term>Genetic Complementation Test</term><term>Host-Pathogen Interactions</term><term>Membrane Glycoproteins (biosynthesis)</term><term>Membrane Glycoproteins (deficiency)</term><term>Mutation</term><term>Receptors, Virus (biosynthesis)</term><term>Receptors, Virus (deficiency)</term><term>Virus Internalization</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Membrane Glycoproteins</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Membrane Glycoproteins</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Ebolavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Ebolavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>CHO Cells</term><term>Cricetinae</term><term>Cricetulus</term><term>Genetic Complementation Test</term><term>Host-Pathogen Interactions</term><term>Mutation</term><term>Virus Internalization</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ebolavirus causes severe hemorrhagic fever in humans and non-human primates. Entry of ebolavirus is mediated by the viral glycoprotein, GP; however, the required host factors have not been fully elucidated. A screen utilizing a recombinant Vesicular Stomatitis Virus (VSV) encoding Zaire ebolavirus GP identified four Chinese Hamster Ovary (CHO) cell lines resistant to GP-mediated viral entry. Susceptibility to vectors carrying SARS coronavirus S or VSV-G glycoproteins suggests that endocytic and processing pathways utilized by other viruses are intact in these cells. A cathepsin-activated form of the ebolaviral glycoprotein did not overcome the entry restriction, nor did expression of several host factors previously described as important for ebolavirus entry. Conversely, expression of the recently described ebolavirus host entry factor Niemann-Pick Type C1 (NPC1) restored infection. Resistant cells encode distinct mutations in the NPC1 gene, resulting in loss of protein expression. These studies reinforce the importance of NPC1 for ebolavirus entry.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22726751</PMID><DateCompleted><Year>2012</Year><Month>10</Month><Day>02</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0341</ISSN><JournalIssue CitedMedium="Internet"><Volume>432</Volume><Issue>1</Issue><PubDate><Year>2012</Year><Month>Oct</Month><Day>10</Day></PubDate></JournalIssue><Title>Virology</Title><ISOAbbreviation>Virology</ISOAbbreviation></Journal><ArticleTitle>Chinese hamster ovary cell lines selected for resistance to ebolavirus glycoprotein mediated infection are defective for NPC1 expression.</ArticleTitle><Pagination><MedlinePgn>20-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virol.2012.05.018</ELocationID><Abstract><AbstractText>Ebolavirus causes severe hemorrhagic fever in humans and non-human primates. Entry of ebolavirus is mediated by the viral glycoprotein, GP; however, the required host factors have not been fully elucidated. A screen utilizing a recombinant Vesicular Stomatitis Virus (VSV) encoding Zaire ebolavirus GP identified four Chinese Hamster Ovary (CHO) cell lines resistant to GP-mediated viral entry. Susceptibility to vectors carrying SARS coronavirus S or VSV-G glycoproteins suggests that endocytic and processing pathways utilized by other viruses are intact in these cells. A cathepsin-activated form of the ebolaviral glycoprotein did not overcome the entry restriction, nor did expression of several host factors previously described as important for ebolavirus entry. Conversely, expression of the recently described ebolavirus host entry factor Niemann-Pick Type C1 (NPC1) restored infection. Resistant cells encode distinct mutations in the NPC1 gene, resulting in loss of protein expression. These studies reinforce the importance of NPC1 for ebolavirus entry.</AbstractText><CopyrightInformation>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Haines</LastName><ForeName>Kathleen M</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6076, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vande Burgt</LastName><ForeName>Nathan H</ForeName><Initials>NH</Initials></Author><Author ValidYN="Y"><LastName>Francica</LastName><ForeName>Joseph R</ForeName><Initials>JR</Initials></Author><Author ValidYN="Y"><LastName>Kaletsky</LastName><ForeName>Rachel L</ForeName><Initials>RL</Initials></Author><Author ValidYN="Y"><LastName>Bates</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 AI007324</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32AI055400</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54AI57168</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI081913</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01AI081913</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 AI070369</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 AI057168</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32AI007324</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI055400</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Virology</MedlineTA><NlmUniqueID>0110674</NlmUniqueID><ISSNLinking>0042-6822</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016466" 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