DC-SIGN and DC-SIGNR bind ebola glycoproteins and enhance infection of macrophages and endothelial cells
- PMID: 12504546
- DOI: 10.1006/viro.2002.1730
DC-SIGN and DC-SIGNR bind ebola glycoproteins and enhance infection of macrophages and endothelial cells
Abstract
Ebola virus exhibits a broad cellular tropism in vitro. In humans and animal models, virus is found in most tissues and organs during the latter stages of infection. In contrast, a more restricted cell and tissue tropism is exhibited early in infection where macrophages, liver, lymph node, and spleen are major initial targets. This indicates that cellular factors other than the broadly expressed virus receptor(s) modulate Ebola virus tropism. Here we demonstrate that the C-type lectins DC-SIGN and DC-SIGNR avidly bind Ebola glycoproteins and greatly enhance transduction of primary cells by Ebola virus pseudotypes and infection by replication-competent Ebola virus. DC-SIGN and DC-SIGNR are expressed in several early targets for Ebola virus infection, including dendritic cells, alveolar macrophages, and sinusoidal endothelial cells in the liver and lymph node. While DC-SIGN and DC-SIGNR do not directly mediate Ebola virus entry, their pattern of expression in vivo and their ability to efficiently capture virus and to enhance infection indicate that these attachment factors can play an important role in Ebola transmission, tissue tropism, and pathogenesis.
Similar articles
-
Analysis of the interaction of Ebola virus glycoprotein with DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) and its homologue DC-SIGNR.J Infect Dis. 2007 Nov 15;196 Suppl 2(Suppl 2):S237-46. doi: 10.1086/520607. J Infect Dis. 2007. PMID: 17940955 Free PMC article.
-
West Nile virus discriminates between DC-SIGN and DC-SIGNR for cellular attachment and infection.J Virol. 2006 Feb;80(3):1290-301. doi: 10.1128/JVI.80.3.1290-1301.2006. J Virol. 2006. PMID: 16415006 Free PMC article.
-
DC-SIGN: binding receptors for hepatitis C virus.Chin Med J (Engl). 2004 Sep;117(9):1395-400. Chin Med J (Engl). 2004. PMID: 15377434 Review.
-
Hepatitis C virus glycoproteins interact with DC-SIGN and DC-SIGNR.J Virol. 2003 Apr;77(7):4070-80. doi: 10.1128/jvi.77.7.4070-4080.2003. J Virol. 2003. PMID: 12634366 Free PMC article.
-
The role of DC-SIGN and DC-SIGNR in HIV and Ebola virus infection: can potential therapeutics block virus transmission and dissemination?Expert Opin Ther Targets. 2002 Aug;6(4):423-31. doi: 10.1517/14728222.6.4.423. Expert Opin Ther Targets. 2002. PMID: 12223058 Review.
Cited by
-
Common pathways targeted by viral hemorrhagic fever viruses to infect the placenta and increase the risk of stillbirth.Placenta. 2023 Sep 26;141:2-9. doi: 10.1016/j.placenta.2022.10.002. Epub 2022 Oct 14. Placenta. 2023. PMID: 36939178
-
Pseudotyped Viruses for Marburgvirus and Ebolavirus.Adv Exp Med Biol. 2023;1407:105-132. doi: 10.1007/978-981-99-0113-5_6. Adv Exp Med Biol. 2023. PMID: 36920694
-
Tinker, tailor, soldier, cell: the role of C-type lectins in the defense and promotion of disease.Protein Cell. 2022 Jul 15;14(1):4-16. doi: 10.1093/procel/pwac012. eCollection 2023 Jan. Protein Cell. 2022. PMID: 36726757 Free PMC article. Review.
-
Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines.Pathogens. 2022 Nov 23;11(12):1400. doi: 10.3390/pathogens11121400. Pathogens. 2022. PMID: 36558734 Free PMC article. Review.
-
Macrophage infection, activation, and histopathological findings in ebolavirus infection.Front Cell Infect Microbiol. 2022 Oct 12;12:1023557. doi: 10.3389/fcimb.2022.1023557. eCollection 2022. Front Cell Infect Microbiol. 2022. PMID: 36310868 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases
Miscellaneous