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Journal of Virology, August 2005, p. 10397-10407, Vol. 79, No. 16
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.16.10397-10407.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Vaccinia Virus Tropism for Primary Hematolymphoid Cells Is Determined by Restricted Expression of a Unique Virus Receptor

Ann Chahroudi,1 Rahul Chavan,1 Natalia Koyzr,1 Edmund K. Waller,2 Guido Silvestri,1 and Mark B. Feinberg1*

Emory Vaccine Center,1 Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 303292

Received 1 December 2004/ Accepted 6 April 2005

The presumed broad tropism of poxviruses has stymied attempts to identify both the cellular receptor(s) and the viral determinant(s) for binding. Detailed studies of poxvirus binding to and infection of primary human cells have not been conducted. In particular, the determinants of target cell infection and the consequences of infection for cells involved in the generation of antiviral immune responses are incompletely understood. In this report, we show that vaccinia virus (VV) exhibits a more restricted tropism for primary hematolymphoid human cells than has been previously recognized. We demonstrate that vaccinia virus preferentially infects antigen-presenting cells (dendritic cells, monocytes/macrophages, and B cells) and activated T cells, but not resting T cells. The infection of activated T cells is permissive, with active viral replication and production of infectious progeny. Susceptibility to infection is determined by restricted expression of a cellular receptor that is induced de novo upon T-cell activation and can be removed from the cell surface by either trypsin or pronase treatment. The VV receptor expressed on activated T cells displays unique characteristics that distinguish it from the receptor used to infect cell lines in culture. The observed restricted tropism of VV may have significant consequences for the understanding of natural poxvirus infection and immunity and for poxvirus-based vaccine development.

* Corresponding author. Present address: Merck Vaccine Division, WP97-A337, 770 Sumneytown Pike, P.O. Box 4, West Point, PA 19486. Phone: (215) 652-8664, Fax: (215) 652-8918. E-mail: mark_feinberg{at}merck.com.

Journal of Virology, August 2005, p. 10397-10407, Vol. 79, No. 16
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.16.10397-10407.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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