Links for fulltext
     (May Require Subscription)
Supplementary

Article: Identification of major histocompatibility complex class I C molecule as an attachment factor that facilitates coronavirus HKU1 spike-mediated infection

TitleIdentification of major histocompatibility complex class I C molecule as an attachment factor that facilitates coronavirus HKU1 spike-mediated infection
Authors
Issue Date2009
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2009, v. 83 n. 2, p. 1026-1035 How to Cite?
AbstractHuman coronavirus HKU1 (HCoV-HKU1) is a recently discovered human coronavirus associated with respiratory tract infections worldwide. In this study, we have identified the major histocompatibility complex class I C molecule (HLA-C) as an attachment factor in facilitating HCoV-HKU1 spike (S)-mediated infection. HCoV-HKU1 S pseudotyped virus was assembled using a human immunodeficiency virus type 1-derived reporter virus harboring the human codon-optimized spike of HCoV-HKU1. We identified human alveolar epithelial A549 cells as the most susceptible cell line among those tested to infection by HCoV-HKU1 S pseudotypes. A549 cells were shown to bind purified soluble HCoV-HKU1 S1-600 glycopeptide. To search for the functional receptor for HCoV-HKU1, an A549 cDNA expression library was constructed and transduced into the nonpermissive, baby hamster kidney cells line BHK-21. Transduced cells that bind soluble HCoV-HKU1 S1-600 glycoprotein with C-terminal FLAG were sorted. Sequencing of two independent clones revealed cDNA inserts encoding HLA-C. Inhibition of HLA-C expression or function by RNAi silencing and anti-HLA-C antibody decreased HCoV-HKU1 S pseudotyped virus infection of A549 cells by 62 to 65%, whereas pretreatment of cells with neuraminidase decreased such infection by only 13%. When HLA-C was constitutively expressed in another nonpermissive cell line, NIH-3T3, quantitative PCR showed that the binding of HCoV-HKU1 S pseudotyped virus to cell surfaces was increased by 200-fold, but the cells remained nonsusceptible to HCoV-HKU1 S pseudotyped virus infection. Our data suggest that HLA-C is involved in the attachment of HCoV-HKU1 to A549 cells and is a potential candidate to facilitate cell entry. However, other unknown surface proteins on A549 cells may be concomitantly utilized by S glycoprotein of HCoV-HKU1 during viral entry. Further studies are required to elucidate other putative receptors or coreceptors for HCoV-HKU1 and the mechanism of HCoV-HKU1 S-mediated cell entry. Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/68296
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Special Administrative Region Research Fund for the Control of Infectious Diseases of the Health, Welfare, and Food Bureau
Hong Kong University Special Research Achievement Award
Research Grant CouncilGRF 781008 M
Funding Information:

This work is supported by Richard Yu and Carol Yu, the Hong Kong Special Administrative Region Research Fund for the Control of Infectious Diseases of the Health, Welfare, and Food Bureau, the Hong Kong University Special Research Achievement Award, and the Research Grant Council (GRF 781008 M).

References

 

DC FieldValueLanguage
dc.contributor.authorChan, CMen_HK
dc.contributor.authorLau, SKPen_HK
dc.contributor.authorWoo, PCYen_HK
dc.contributor.authorTse, Hen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorHuang, JDen_HK
dc.contributor.authorYuen, KYen_HK
dc.date.accessioned2010-09-06T06:03:14Z-
dc.date.available2010-09-06T06:03:14Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Virology, 2009, v. 83 n. 2, p. 1026-1035en_HK
dc.identifier.issn0022-538Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/68296-
dc.description.abstractHuman coronavirus HKU1 (HCoV-HKU1) is a recently discovered human coronavirus associated with respiratory tract infections worldwide. In this study, we have identified the major histocompatibility complex class I C molecule (HLA-C) as an attachment factor in facilitating HCoV-HKU1 spike (S)-mediated infection. HCoV-HKU1 S pseudotyped virus was assembled using a human immunodeficiency virus type 1-derived reporter virus harboring the human codon-optimized spike of HCoV-HKU1. We identified human alveolar epithelial A549 cells as the most susceptible cell line among those tested to infection by HCoV-HKU1 S pseudotypes. A549 cells were shown to bind purified soluble HCoV-HKU1 S1-600 glycopeptide. To search for the functional receptor for HCoV-HKU1, an A549 cDNA expression library was constructed and transduced into the nonpermissive, baby hamster kidney cells line BHK-21. Transduced cells that bind soluble HCoV-HKU1 S1-600 glycoprotein with C-terminal FLAG were sorted. Sequencing of two independent clones revealed cDNA inserts encoding HLA-C. Inhibition of HLA-C expression or function by RNAi silencing and anti-HLA-C antibody decreased HCoV-HKU1 S pseudotyped virus infection of A549 cells by 62 to 65%, whereas pretreatment of cells with neuraminidase decreased such infection by only 13%. When HLA-C was constitutively expressed in another nonpermissive cell line, NIH-3T3, quantitative PCR showed that the binding of HCoV-HKU1 S pseudotyped virus to cell surfaces was increased by 200-fold, but the cells remained nonsusceptible to HCoV-HKU1 S pseudotyped virus infection. Our data suggest that HLA-C is involved in the attachment of HCoV-HKU1 to A549 cells and is a potential candidate to facilitate cell entry. However, other unknown surface proteins on A549 cells may be concomitantly utilized by S glycoprotein of HCoV-HKU1 during viral entry. Further studies are required to elucidate other putative receptors or coreceptors for HCoV-HKU1 and the mechanism of HCoV-HKU1 S-mediated cell entry. Copyright © 2009, American Society for Microbiology. All Rights Reserved.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_HK
dc.relation.ispartofJournal of Virologyen_HK
dc.rightsJournal of Virology. Copyright © American Society for Microbiology.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCoronavirus - physiologyen_HK
dc.subject.meshCricetinaeen_HK
dc.subject.meshEpithelial Cells - virologyen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshHLA-C Antigens - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMembrane Glycoproteins - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshReceptors, Virus - genetics - metabolismen_HK
dc.subject.meshViral Envelope Proteins - metabolismen_HK
dc.subject.meshVirus Attachmenten_HK
dc.titleIdentification of major histocompatibility complex class I C molecule as an attachment factor that facilitates coronavirus HKU1 spike-mediated infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-538X&volume=83&spage=1026&epage=1035&date=2009&atitle=Identification+Of+Major+Histocompatibility+Complex+Class+I+C+Molecule+As+An+Attachment+Factor+That+Facilitates+Coronavirus+Hku1+Spike-mediated+Infectionen_HK
dc.identifier.emailLau, SKP:skplau@hkucc.hku.hken_HK
dc.identifier.emailWoo, PCY:pcywoo@hkucc.hku.hken_HK
dc.identifier.emailTse, H:herman@graduate.hku.hken_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.authorityLau, SKP=rp00486en_HK
dc.identifier.authorityWoo, PCY=rp00430en_HK
dc.identifier.authorityTse, H=rp00519en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityHuang, JD=rp00451en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.01387-08en_HK
dc.identifier.pmid18987136-
dc.identifier.pmcidPMC2612401-
dc.identifier.scopuseid_2-s2.0-58149487662en_HK
dc.identifier.hkuros161669en_HK
dc.identifier.hkuros156483-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58149487662&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume83en_HK
dc.identifier.issue2en_HK
dc.identifier.spage1026en_HK
dc.identifier.epage1035en_HK
dc.identifier.isiWOS:000262045000049-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChe, MC=25957922600en_HK
dc.identifier.scopusauthoridLau, SKP=7401596211en_HK
dc.identifier.scopusauthoridWoo, PCY=7201801340en_HK
dc.identifier.scopusauthoridTse, H=7006070596en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridChen, L=7409435006en_HK
dc.identifier.scopusauthoridHuang, JD=8108660600en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats