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Published ahead of print on November 11, 2005, doi:10.1165/rcmb.2005-0287OC
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American Journal of Respiratory Cell and Molecular Biology. Vol. 34, pp. 320-329, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2005-0287OC

Differential Response of Dendritic Cells to Human Metapneumovirus and Respiratory Syncytial Virus

Antonieta Guerrero-Plata, Antonella Casola, Giovanni Suarez, Xiang Yu, LeAnne Spetch, Mark E. Peeples and Roberto P. Garofalo

Departments of Pediatrics, Microbiology & Immunology, and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas; and Department of Pediatrics, Ohio State University, Columbus, Ohio

Correspondence and requests for reprints should be addressed to Roberto P. Garofalo, M.D., Department of Pediatrics, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0369. E-mail: rpgarofa{at}utmb.edu

Dendritic cells (DCs) play a pivotal role in shaping antiviral immune responses in the respiratory tract. Human metapneumovirus (hMPV) is a recently identified pathogen and like its better known relative, respiratory syncytial virus (RSV), has been increasingly recognized as a major cause of respiratory morbidity in infants and in elderly persons. In the present study, we examined susceptibility as well as cellular responses of human DCs to hMPV compared with RSV. Monocyte-derived DCs (moDCs) were susceptible to infection by both viruses, but only RSV was able to induce a productive infection with release of viral progeny. Despite the fact that viral infection resulted in phenotypic maturation of moDCs, as shown by the upregulation of cell surface markers and antigen-presenting molecules (MHC I and II, CD80, CD83, CD86, CD38), RSV-infected moDCs showed a severely impaired capacity to stimulate CD4+ T cell proliferation. Compared with hMPV, RSV was a more potent inducer of inflammatory and immunomodulatory cytokines, including TNF-{alpha}, IL-6, IL-1beta, IL-10, and IL-12p70 in both moDCs and plasmacytoid dendritic cells (pDCs). On the other hand, hMPV, but not RSV, was able to trigger production of IFN-{alpha} by moDCs, while both viruses strongly induced IFN-{alpha} in pDCs. Finally, both viruses strikingly suppressed IFN-{alpha} production by moDCs or pDCs stimulated with synthetic dsRNA and CpG-ODN, respectively. The findings provide novel evidence that RSV and hMPV differentially activate human DCs and may use distinct mechanisms to interfere with the host innate and adaptive immune responses.

Key Words: dendritic cells • respiratory syncytial virus • human metapneumovirus • interferon type I • innate immunity




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