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Hydroxyurea interferes with antigen-dependent T-cell activation in vitro.

J M Orendi¹, H S Nottet, N M De Vos

¹University Medical Center, Utrecht; Leiden University Medical Center, Leiden, The Netherlands. orendi@microbiology.azl.nl

European Journal of Clinical Investigation

|January 29, 2000

Summary

Hydroxyurea inhibits T-cell activation at low concentrations, suggesting a novel mechanism for its anti-HIV-1 effects beyond reducing deoxynucleotides. This impacts HIV target cell numbers in vivo.

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Area of Science:

Immunology
Virology
Pharmacology

Background:

Hydroxyurea is thought to inhibit HIV-1 by depleting deoxynucleotides essential for viral replication.
A safe plasma concentration of 400 micromol L-1 is established in oncology.
This study investigates hydroxyurea's interference with antigen-dependent T-cell activation as a potential HIV inhibition mechanism.

Purpose of the Study:

To explore hydroxyurea's impact on antigen-induced T-cell activation.
To determine if hydroxyurea affects T-cell proliferation at concentrations relevant to HIV-1 inhibition.

Main Methods:

Peripheral blood mononuclear cells (PBMC) were used for in vitro studies.
The effect of hydroxyurea on common antigen-induced cell proliferation was assessed.

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Main Results:

Hydroxyurea inhibited Candida albicans-induced PBMC proliferation at 1 micromol L-1.
Blocking HIV-1 replication in PHA-stimulated PBMC required at least 10 micromol L-1 hydroxyurea.

Conclusions:

Hydroxyurea inhibits antigen-induced lymphoproliferation in vitro at concentrations that do not inhibit PHA-induced HIV replication.
Hydroxyurea may inhibit HIV-1 by interfering with antigen-dependent T-cell activation, reducing target cell numbers in CD4+ T cells.
This suggests a dual mechanism for hydroxyurea's anti-HIV-1 activity in vivo.