The ssRNA genome of human rhinovirus induces a type I IFN response but fails to induce maturation in human monocyte-derived dendritic cells.

Dendritic cells (DCs) use pattern recognition receptors to sense invading viruses and triggering of these receptors induces a maturation program. Human rhinoviruses (HRVs) belong to the family of Picornaviridae, which have a single-stranded, coding RNA genome. Because HRV does not replicate in DCs, we used genomic RNA from HRV in this study to analyze the impact of natural occurring viral ssRNA on DC function. We found that transfection of human monocyte-derived DCs with viral ssRNA induced type I IFN production but failed to activate the NF-kappaB pathway in DCs. In line with this observation, the up-regulation of typical maturation markers such as CD83 or the production of the proinflammatory cytokines IL-12p40, IL-6, and TNF-alpha was not detectable. Most importantly, the T cell stimulatory capacity of viral ssRNA-treated DCs was not enhanced and remained at the level of immature DCs. Taken together, our results demonstrate that viral ssRNA efficiently activates the innate defense arm of DCs, whereas it is insufficient to activate the stimulatory capacity of DCs for the adaptive defense responses.