American Society for Microbiology, Journal of Virology, 9(84), p. 4845-4850, 2010
DOI: 10.1128/jvi.02514-09
American Society for Microbiology, Journal of Virology, 6(85), p. 3042-3042, 2011
DOI: 10.1128/jvi.00100-11
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ABSTRACT Dengue virus (DENV) infects human immune cells in vitro and likely infects dendritic cells (DCs) in vivo . DENV-2 productive infection induces activation and release of high levels of chemokines and proinflammatory cytokines in monocyte-derived DCs (moDCs), with the notable exception of alpha/beta interferon (IFN-α/β). Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack of IFN-α/β released by moDCs, since this effect was reversed by addition of exogenous IFN-β. Together, our data show that inhibition of IFN-α/β production by DENV in primary human moDCs is a novel mechanism of immune evasion.