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Journal of Virology, December 2007, p. 13640-13648, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.00857-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Differential Activation of Human Monocyte-Derived and Plasmacytoid Dendritic Cells by West Nile Virus Generated in Different Host Cells{triangledown}

Maria Carlan Silva,1,{dagger} Antonieta Guerrero-Plata,2,{dagger} Felicia D. Gilfoy,1 Roberto P. Garofalo,2,3,4 and Peter W. Mason1,3,4*

Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555,1 Department of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77555,2 Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas 77555,3 Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 775554

Received 22 April 2007/ Accepted 18 September 2007

Dendritic cells (DCs) play a central role in innate immunity and antiviral responses. In this study, we investigated the production of alpha interferon (IFN-{alpha}) and inducible chemokines by human monocyte-derived dendritic cells (mDCs) and plasmacytoid dendritic cells (pDCs) infected with West Nile virus (WNV), an emergent pathogen whose infection can lead to severe cases of encephalitis in the elderly, children, and immunocompromised individuals. Our experiments demonstrated that WNV grown in mammalian cells (WNVVero) was a potent inducer of IFN-{alpha} secretion in pDCs and, to a lesser degree, in mDCs. The ability of WNVVero to induce IFN-{alpha} in pDCs did not require viral replication and was prevented by the treatment of cells with bafilomycin A1 and chloroquine, suggesting that it was dependent on endosomal Toll-like receptor recognition. On the other hand, IFN-{alpha} production in mDCs required viral replication and was associated with the nuclear translocation of IRF3 and viral antigen expression. Strikingly, pDCs failed to produce IFN-{alpha} when stimulated with WNV grown in mosquito cells (WNVC7/10), while mDCs responded similarly to WNVVero or WNVC7/10. Moreover, the IFN-dependent chemokine IP-10 was produced in substantial amounts by pDCs in response to WNVVero but not WNVC7/10, while interleukin-8 was produced in greater amounts by mDCs infected with WNVC7/10 than in those infected with WNVVero. These findings suggest that cell-specific mechanisms of WNV recognition leading to the production of type I IFN and inflammatory chemokines by DCs may contribute to both the innate immune response and disease pathogenesis in human infections.

* Corresponding author. Mailing address: Department of Pathology, 3.206B Mary Moody Northen Pavilion, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0436. Phone: (409) 747-8143. Fax: (409) 747-8150. E-mail: pwmason{at}utmb.edu

{triangledown} Published ahead of print on 3 October 2007.

{dagger} M.C.S. and A.G.-P. contributed equally to this work.

Journal of Virology, December 2007, p. 13640-13648, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.00857-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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