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Beyond attachment: Roles of DC-SIGN in dengue virus infection.
Traffic. 2017 04; 18(4):218-231.T

Abstract

Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), a C-type lectin expressed on the plasma membrane by human immature dendritic cells, is a receptor for numerous viruses including Ebola, SARS and dengue. A controversial question has been whether DC-SIGN functions as a complete receptor for both binding and internalization of dengue virus (DENV) or whether it is solely a cell surface attachment factor, requiring either hand-off to another receptor or a co-receptor for internalization. To examine this question, we used 4 cell types: human immature dendritic cells and NIH3T3 cells expressing either wild-type DC-SIGN or 2 internalization-deficient DC-SIGN mutants, in which either the 3 cytoplasmic internalization motifs are silenced by alanine substitutions or the cytoplasmic region is truncated. Using confocal and super-resolution imaging and high content single particle tracking, we investigated DENV binding, DC-SIGN surface transport, endocytosis, as well as cell infectivity. DC-SIGN was found colocalized with DENV inside cells suggesting hand-off at the plasma membrane to another receptor did not occur. Moreover, all 3 DC-SIGN molecules on NIH3T3 cells supported cell infection. These results imply the involvement of a co-receptor because cells expressing the internalization-deficient mutants could still be infected.

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Authors+Show Affiliations

Liu P
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Ridilla M
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Patel P
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Betts L
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Gallichotte E
Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Shahidi L
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Thompson NL
Department of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Jacobson K
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

MeSH

AnimalsCell Adhesion MoleculesCell LineCell MembraneDendritic CellsDengueDengue VirusEndocytosisLectins, C-TypeMiceNIH 3T3 CellsReceptors, Cell Surface

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28128492

Citation

Liu, Ping, et al. "Beyond Attachment: Roles of DC-SIGN in Dengue Virus Infection." Traffic (Copenhagen, Denmark), vol. 18, no. 4, 2017, pp. 218-231.
Liu P, Ridilla M, Patel P, et al. Beyond attachment: Roles of DC-SIGN in dengue virus infection. Traffic. 2017;18(4):218-231.
Liu, P., Ridilla, M., Patel, P., Betts, L., Gallichotte, E., Shahidi, L., Thompson, N. L., & Jacobson, K. (2017). Beyond attachment: Roles of DC-SIGN in dengue virus infection. Traffic (Copenhagen, Denmark), 18(4), 218-231. https://doi.org/10.1111/tra.12469
Liu P, et al. Beyond Attachment: Roles of DC-SIGN in Dengue Virus Infection. Traffic. 2017;18(4):218-231. PubMed PMID: 28128492.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beyond attachment: Roles of DC-SIGN in dengue virus infection. AU - Liu,Ping, AU - Ridilla,Marc, AU - Patel,Pratik, AU - Betts,Laurie, AU - Gallichotte,Emily, AU - Shahidi,Lidea, AU - Thompson,Nancy L, AU - Jacobson,Ken, Y1 - 2017/02/28/ PY - 2015/05/18/received PY - 2017/01/24/revised PY - 2017/01/24/accepted PY - 2017/1/28/pubmed PY - 2017/9/16/medline PY - 2017/1/28/entrez KW - DC-SIGN KW - C-type lectin receptor KW - antigen-presenting cells KW - dengue virus KW - fluorescence microscopy KW - in vivo trafficking KW - quantitative colocalization KW - super-resolution imaging KW - viral entry KW - viral receptor SP - 218 EP - 231 JF - Traffic (Copenhagen, Denmark) JO - Traffic VL - 18 IS - 4 N2 - Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), a C-type lectin expressed on the plasma membrane by human immature dendritic cells, is a receptor for numerous viruses including Ebola, SARS and dengue. A controversial question has been whether DC-SIGN functions as a complete receptor for both binding and internalization of dengue virus (DENV) or whether it is solely a cell surface attachment factor, requiring either hand-off to another receptor or a co-receptor for internalization. To examine this question, we used 4 cell types: human immature dendritic cells and NIH3T3 cells expressing either wild-type DC-SIGN or 2 internalization-deficient DC-SIGN mutants, in which either the 3 cytoplasmic internalization motifs are silenced by alanine substitutions or the cytoplasmic region is truncated. Using confocal and super-resolution imaging and high content single particle tracking, we investigated DENV binding, DC-SIGN surface transport, endocytosis, as well as cell infectivity. DC-SIGN was found colocalized with DENV inside cells suggesting hand-off at the plasma membrane to another receptor did not occur. Moreover, all 3 DC-SIGN molecules on NIH3T3 cells supported cell infection. These results imply the involvement of a co-receptor because cells expressing the internalization-deficient mutants could still be infected. SN - 1600-0854 UR - https://www.unboundmedicine.com/medline/citation/28128492/Beyond_attachment:_Roles_of_DC_SIGN_in_dengue_virus_infection_ DB - PRIME DP - Unbound Medicine ER -