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Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection

Center for Vaccines and Immunity, Columbus Children's Research Institute, Columbus Children's Hospital, Columbus, Ohio 43205,¹ The Ohio State University College of Medicine, Columbus, Ohio,² Instituto de Medicina Molecular, Universidade de Lisboa, Lisboa, and Instituto Gulbenkian de Ciência, Oeiras, Portugal³

Received 19 February 2007/ Accepted 22 June 2007

The respiratory tract is a major mucosal site for microorganism entry into the body, and type I interferon (IFN) and dendritic cells constitute a first line of defense against viral infections. We have analyzed the interaction between a model DNA virus, plasmacytoid dendritic cells, and type I IFN during lung infection of mice. Our data show that murine gammaherpesvirus 68 (HV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to HV68. Following HV68 intranasal inoculation, the local and systemic IFN-/ß response is below detectable levels, and plasmacytoid dendritic cells are activated and recruited into the lung with a tissue distribution that differs from that of conventional dendritic cells. Our results suggest that plasmacytoid dendritic cells and type I IFN have important but independent roles during the early response to a respiratory HV68 infection. HV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-/ß in vivo, which may serve as an immune evasion strategy.

Published ahead of print on 11 July 2007.