Production of interleukin-1 (IL-1) and IL-1 inhibitor by human monocytes exposed to dengue virus.

Abstract

Dengue hemorrhagic fever-dengue shock syndrome, the most severe manifestation of an acute dengue virus (DV) infection, is endemic in Southeast Asia. Antibody-dependent enhancement of DV growth in mononuclear phagocytes is thought to be the mechanism whereby preexisting dengue antibodies confer excess risk for this outcome. Interleukin-1 (IL-1) may play an important role in the pathogenetic mechanisms that cause dengue fever and shock. It was shown that both IL-1 and tumor necrosis factor-alpha are secreted from monocytes within 4 h after DV infection. However, there was no increase in IL-1 secretion by virus-stimulated monocytes from dengue fever patients compared with healthy controls. Significant amounts of IL-1 were secreted by DV-infected monocytes in the presence of aggregated immunoglobulin or immune complexes. In addition, a new 600-kDa IL-1 inhibitor from the supernatants of DV-infected monocytes was identified. This inhibitor may cause immunosuppression and influence the process of DV infection.