Human immunodeficiency virus type 1 replication inhibition by the bidentate iron chelators CP502 and CP511 is caused by proliferation inhibition and the onset of apoptosis

Eur J Clin Invest. 2002 Mar:32 Suppl 1:91-6. doi: 10.1046/j.1365-2362.2002.0320s1091.x.

Abstract

Background: The iron chelators deferoxamine (DF) and deferiprone (CP20) have been shown to inhibit human immunodeficiency virus type 1 (HIV-1) replication in human peripheral blood lymphocytes (PBL). The orally active bidentate chelators CP502 and CP511, which also belong to the 3-hydroxypyridin-4-one family, but with higher affinities for iron than CP20, were monitored for their antiviral properties by checking for p24 antigen production and nuclear factor (NF)-kappaB activation, and their ability to induce apoptosis.

Materials and methods: Human PBLs were isolated from HIV-1 seronegative donors and subsequently infected with HIV-1(Ba-L) for 2 h. After 5 days' incubation, HIV-1 replication was monitored by p24 antigen production. Cellular proliferation as well as caspase-3 activity were monitored in uninfected cells after a period of 5 days and after 1 day infection, respectively. NF-kappaB activity was also monitored by electromobility shift assays (EMSA) performed on nuclear extracts of Jurkat cells treated with the different chelators for 4 h.

Results: CP502 and CP511 decrease HIV-1 replication by decreasing cellular proliferation in a similar manner to DF and CP20. CP511 seemed to be more potent than either CP502 or CP20. Due to the reduction in cellular proliferation, there was an increase in caspase-3 activity after 24 h incubation. NF-kappaB activity was not affected by any of the chelators.

Conclusions: Iron chelators with high affinities for iron, which are under development for the treatment of iron overload, could contribute to the reduction of HIV-1 replication in infected patients by cellular proliferation inhibition rather than by a direct antiviral action.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / immunology
  • Caspase 3
  • Caspases / metabolism
  • Cell Division / drug effects
  • Cell Division / immunology
  • Deferiprone
  • HIV Infections / drug therapy
  • HIV-1 / growth & development*
  • Humans
  • Iron Chelating Agents / pharmacology*
  • Jurkat Cells
  • Lymphocytes / cytology
  • Lymphocytes / drug effects
  • Lymphocytes / virology
  • NF-kappa B / metabolism
  • Pyridones / pharmacology*
  • Virus Replication / drug effects*

Substances

  • Iron Chelating Agents
  • NF-kappa B
  • Pyridones
  • Deferiprone
  • CASP3 protein, human
  • Caspase 3
  • Caspases