Scientific Publications by FDA Staff

Biochem Biophys Res Commun 2016 May 13;473(4):926-30

IL-1beta and IL-18 Inhibition of HIV-1 Replication in Jurkat Cells and PBMCs.

Wang X, Mbondji-Wonje C, Zhao J, Hewlett I

HIV-1 infection-induced apoptosis is able to ensure viral replication. The death of some CD4+ T cells residing in lymphoid tissues can be induced by HIV-1 infection through caspase-1 driven pyroptosis with release of cytokine of IL-1ß and IL-18. It is not well known whether IL-1ß and IL-18 affect HIV-1 replication in lymphocytic cells. Using susceptible lymphocytic cell line, Jurkat cells, and primary peripheral blood mononuclear cells (PBMCs), we studied the effects of IL-1ß and IL-18 on HIV-1 replication. We found that treatment with exogenous IL-1ß protein (rIL-1ß) and IL-18 protein (rIL-18), or expression of IL-1ß and IL-18 significantly reduced HIV-1 replication. HIV-1 infection enhanced caspase-3 expression and its activation, and had no effects on caspase-1 activity. Treatment with rIL-1ß and rIL-18 dramatically lowered caspase-3 activity. IL-1ß and IL-18 also played roles in diminishing reactivation of viral replication from latency in J1.1 cells. These results indicate that IL-1ß and IL-18 are able to inhibit HIV-1 replication, and their effects may be due to signaling through apoptosis involved in inactivation of caspase-3 activity.