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Article: Lectin switching during dengue virus infection

TitleLectin switching during dengue virus infection
Authors
Issue Date2011
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2011, v. 203 n. 12, p. 1775-1783 How to Cite?
AbstractDengue virus receptors are relatively poorly characterized, but there has been recent interest in 2 C-type lectin molecules, dendritic cell-specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) and its close homologue liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN), which can both bind dengue and promote infection. In this report we have studied the interaction of dengue viruses produced in insect cells, tumor cell lines, and primary human dendritic cells (DCs) with DC-SIGN and L-SIGN. Virus produced in primary DCs is unable to interact with DC-SIGN but remains infectious for L-SIGN-expressing cells. Skin-resident DCs may thus be a site of initial infection by insect-produced virus, but DCs will likely not participate in large-scale virus replication during dengue infection. These results reveal that differential glycosylation of dengue virus envelope protein is highly dependent on cell state and suggest that studies of virus tropism using virus prepared in insect cells or tumor cell lines should be interpreted with caution. © The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/135238
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Medical Research Council, UK
Wellcome Trust
Funding Information:

This work was supported by the Medical Research Council, UK, and the Wellcome Trust. A. I. W. is a National Health and Medical Research Council C. J. Martin Fellow.

References

 

DC FieldValueLanguage
dc.contributor.authorDejnirattisai, Wen_HK
dc.contributor.authorWebb, AIen_HK
dc.contributor.authorChan, Ven_HK
dc.contributor.authorJumnainsong, Aen_HK
dc.contributor.authorDavidson, Aen_HK
dc.contributor.authorMongkolsapaya, Jen_HK
dc.contributor.authorScreaton, Gen_HK
dc.date.accessioned2011-07-27T01:30:27Z-
dc.date.available2011-07-27T01:30:27Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2011, v. 203 n. 12, p. 1775-1783en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135238-
dc.description.abstractDengue virus receptors are relatively poorly characterized, but there has been recent interest in 2 C-type lectin molecules, dendritic cell-specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) and its close homologue liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN), which can both bind dengue and promote infection. In this report we have studied the interaction of dengue viruses produced in insect cells, tumor cell lines, and primary human dendritic cells (DCs) with DC-SIGN and L-SIGN. Virus produced in primary DCs is unable to interact with DC-SIGN but remains infectious for L-SIGN-expressing cells. Skin-resident DCs may thus be a site of initial infection by insect-produced virus, but DCs will likely not participate in large-scale virus replication during dengue infection. These results reveal that differential glycosylation of dengue virus envelope protein is highly dependent on cell state and suggest that studies of virus tropism using virus prepared in insect cells or tumor cell lines should be interpreted with caution. © The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.subject.meshAntigens, CD - metabolism-
dc.subject.meshCell Adhesion Molecules - metabolism-
dc.subject.meshDendritic Cells - virology-
dc.subject.meshDengue Virus - metabolism - pathogenicity-
dc.subject.meshLectins - metabolism-
dc.titleLectin switching during dengue virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, V:sfvchan@hku.hken_HK
dc.identifier.authorityChan, V=rp01459en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1093/infdis/jir173en_HK
dc.identifier.pmid21606536-
dc.identifier.pmcidPMC3100511-
dc.identifier.scopuseid_2-s2.0-79957483733en_HK
dc.identifier.hkuros187911en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79957483733&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume203en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1775en_HK
dc.identifier.epage1783en_HK
dc.identifier.eissn1537-6613-
dc.identifier.isiWOS:000291062200011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDejnirattisai, W=6505510584en_HK
dc.identifier.scopusauthoridWebb, AI=7402883203en_HK
dc.identifier.scopusauthoridChan, V=35200370000en_HK
dc.identifier.scopusauthoridJumnainsong, A=16067198100en_HK
dc.identifier.scopusauthoridDavidson, A=7402001807en_HK
dc.identifier.scopusauthoridMongkolsapaya, J=6602451584en_HK
dc.identifier.scopusauthoridScreaton, G=7003284408en_HK

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