Journal
JOURNAL OF VIROLOGY
Volume 84, Issue 9, Pages 4845-4850Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02514-09
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Funding
- Ramon Areces Foundation
- [1R01AI073450-01A2]
- [U19 AI62623]
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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-alpha/beta). Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack of IFN-alpha/beta released by moDCs, since this effect was reversed by addition of exogenous IFN-beta. Together, our data show that inhibition of IFN-alpha/beta production by DENV in primary human moDCs is a novel mechanism of immune evasion.
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