Dengue virus first infects interstitial dcs which, within hours of infection, initiate production of type-i ifns. not only dendritic cells but the majority of dengue virus-infected cells produce ifns (α, β) and type ii (γ) and ifns are crucial for protection against dengue infection in vivo and in vitro
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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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