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

Biochem Biophys Res Commun. 2016 May 13;473(4):926-930. doi: 10.1016/j.bbrc.2016.03.153. Epub 2016 Apr 2.

Abstract

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

Keywords: Caspase-1; Caspase-3; HIV-1; IL-18; IL-1β; Replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caspase 3 / metabolism
  • Cells, Cultured
  • HIV-1 / genetics
  • HIV-1 / physiology*
  • Humans
  • Interleukin-18 / antagonists & inhibitors
  • Interleukin-18 / metabolism
  • Interleukin-18 / physiology*
  • Interleukin-1beta / antagonists & inhibitors
  • Interleukin-1beta / metabolism
  • Interleukin-1beta / physiology*
  • Jurkat Cells
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / virology*
  • Virus Replication*

Substances

  • Interleukin-18
  • Interleukin-1beta
  • Caspase 3