Skip to main content

Controlling the Virus Output Via Urokinase Receptor and Integrin Signaling

We have described that either urokinase-type plasminogen activator (uPA) inhibits HIV expression in monocytic U937 and U1 cell lines (M. Alfano et al., PNAS, 2002, 99:8862-67). We have observed that uPA inhibited HIV expression exclusively when both uPAR and CD18/CD11b (Mac-1) were co-expressed at the cell surface. A second interactor of uPAR, FPRL1, was abundantly expressed on the surface of both unstimulated and stimulated U1 cells; however, peptide antagonists of FPRL1 did not interfere with HIV expression from U1 cells. Incubation of U1 cells with Trojan peptides expressing RhoA domains reversed the anti-HIV activity of uPA. In addition to cell line infection, uPA inhibited in vitro infection of primary monocyte-derived macrophages and virus replication from monocytes of infected individuals cultivated ex-vivo. Thus, RhoA-dependent cytoskeleton rearrangement and intracellular vesicles formation may be related to virion budding and entrapment in intracytoplasmic vacuoles. This is the first report linking integrin activation to a negative control of HIV replication, at least in monocyte/macrophages.

Author information

Affiliations

Authors

Corresponding author

Correspondence to Guido Poli.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Poli, G. Controlling the Virus Output Via Urokinase Receptor and Integrin Signaling. Retrovirology 2, S76 (2005). https://doi.org/10.1186/1742-4690-2-S1-S76

Download citation

Keywords

  • Plasminogen Activator
  • Integrin Signaling
  • Integrin Activation
  • Virus Output
  • Urokinase Receptor