Differential effects of parainfluenza virus type 3 on human monocytes and dendritic cells.

Abstract To understand the lack of protective immunity observed after infection with parainfluenza virus type 3 (PIV3), we tested the effect of the virus on human monocytes and monocyte-derived immature dendritic cells (DCs). Expression of viral antigens on the cell surfaces correlated with replication of the virus, which was marginal in monocytes but extremely efficient in DCs. The virus increased monocyte survival at least in part through the production of granulocyte–macrophage colony-stimulating factor but, in contrast, accelerated DC apoptosis. In addition, PIV3 infection failed to activate monocytes but induced maturation of DCs with increased expression of CD54, HLA-DR, CD86, and CD83 and production of bioactive IL-12. However, PIV3-infected DCs demonstrated low stimulatory properties in DC–T cell cocultures, a finding that could not be attributed to the production of infectious virus or IL-10. These results demonstrate for the first time that PIV3 dramatically modifies the survival and/or the function of antigen-presenting cells and might therefore prevent the development of efficient antiviral immune responses.