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The Journal of Immunology, 2006, 176: 1741-1749.
Copyright © 2006 by The American Association of Immunologists

DC-SIGN Is a Receptor for Human Herpesvirus 8 on Dendritic Cells and Macrophages1

Giovanna Rappocciolo2,*, Frank J. Jenkins*,{dagger}, Heather R. Hensler*, Paolo Piazza*, Mariel Jais*, Luann Borowski*, Simon C. Watkins{ddagger} and Charles R. Rinaldo, Jr*,{dagger}

* Department of Infectious Diseases and Microbiology, Graduate School of Public Health, and {dagger} Department of Pathology and {ddagger} Department of Cell Biology and Physiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261

Human herpesvirus 8 (HHV-8) causes Kaposi’s sarcoma and pleural effusion lymphoma. In this study, we show that dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN; CD209) is a receptor for HHV-8 infection of myeloid DCs and macrophages. DC-SIGN was required for virus attachment to these cells and DC-SIGN-expressing cell lines. HHV-8 binding and infection were blocked by anti-DC-SIGN mAb and soluble DC-SIGN, and mannan, a natural ligand for DC-SIGN. Infection of DCs and macrophages with HHV-8 led to production of viral proteins, with little production of viral DNA, similar to HHV-8 infection of vascular endothelial cells. Infection of DCs resulted in down-regulation of DC-SIGN, a decrease in endocytic activity, and an inhibition of Ag stimulation of CD8+ T cells. We propose that DC-SIGN serves as a portal for immune dysfunction and oncogenesis caused by HHV-8 infection.




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