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Journal of Virology, May 2006, p. 4771-4780, Vol. 80, No. 10
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.10.4771-4780.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

DC-SIGN Facilitates Fusion of Dendritic Cells with Human T-Cell Leukemia Virus Type 1-Infected Cells

Pierre-Emmanuel Ceccaldi,¹ Frédéric Delebecque,² Marie-Christine Prevost,³ Arnaud Moris,² Jean-Pierre Abastado,^4, Antoine Gessain,¹ Olivier Schwartz,² and Simona Ozden^1*

Unité d'Epidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, Paris, France,¹ Groupe Virus et Immunité, Institut Pasteur, Paris, France,² Plate-Forme Microscopie Electronique, Institut Pasteur, Paris, France,³ Immuno Designed Molecules, Paris, France⁴

Received 8 December 2005/ Accepted 16 February 2006

Interactions between the oncogenic retrovirus human T-cell leukemia virus type 1 (HTLV-1) and dendritic cells (DCs) are poorly characterized. We show here that monocyte-derived DCs form syncytia and are infected upon coculture with HTLV-1-infected lymphocytes. We examined the role of DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), a C-type lectin expressed in DCs, in HTLV-1-induced syncytium formation. DC-SIGN is known to bind with high affinity to various viral envelope glycoproteins, including human immunodeficiency virus (HIV) and hepatitis C virus, as well as to the cellular receptors ICAM-2 and ICAM-3. After cocultivating DCs and HTLV-1-infected cells, we found that anti-DC-SIGN monoclonal antibodies (MAbs) were able to decrease the number and size of HTLV-1-induced syncytia. Moreover, expression of the lectin in epithelial-cell lines dramatically enhanced the ability to fuse with HTLV-1-positive cells. Interestingly, in contrast to the envelope (Env) glycoproteins of HIV and other viruses, that of HTLV-1 does not bind directly to DC-SIGN. The facilitating role of the lectin in HTLV-1 syncytium formation is mediated by its interaction with ICAM-2 and ICAM-3, as demonstrated by use of MAbs directed against these adhesion molecules. Altogether, our results indicate that DC-SIGN facilitates HTLV-1 infection and fusion of DCs through an ICAM-dependent mechanism.

Present address: Departement d'Immunologie, Institut Cochin, Paris, France.

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