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pubmed-article:17626106pubmed:abstractTextThe 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 (gammaHV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to gammaHV68. Following gammaHV68 intranasal inoculation, the local and systemic IFN-alpha/beta 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 gammaHV68 infection. gammaHV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-alpha/beta in vivo, which may serve as an immune evasion strategy.lld:pubmed
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pubmed-article:17626106pubmed:authorpubmed-author:DurbinJoan...lld:pubmed
pubmed-article:17626106pubmed:authorpubmed-author:MertzSara ESElld:pubmed
pubmed-article:17626106pubmed:authorpubmed-author:FlañoEmilioElld:pubmed
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pubmed-article:17626106pubmed:articleTitleType I interferon inhibition and dendritic cell activation during gammaherpesvirus respiratory infection.lld:pubmed
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