IL-1β and IL-18 inhibition of HIV-1 replication in Jurkat cells and PBMCs

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-1 beta and IL-18. It is not well known whether IL-1 beta 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-1 beta and IL-18 on HIV-1 replication. We found that treatment with exogenous IL-1 beta protein (rIL-1 beta) and IL-18 protein (rIL-18), or expression of IL-1 beta 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-1 beta and rIL-18 dramatically lowered caspase-3 activity. IL-1 beta and IL-18 also played roles in diminishing reactivation of viral replication from latency in J1.1 cells. These results indicate that IL-1 beta 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. (C) 2016 Elsevier Inc. All rights reserved.