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Open Access Research article

Cultured Kaposi's sarcoma tumor cells exhibit a chemokine receptor repertoire that does not allow infection by HIV-1

Thierry Simonart1, Claire Debussher1, Corinne Liesnard2, Laurent Debaisieux2, Marie-Luce Delforge2, Aurore de Lavareille3, Philippe Hermans5, Jean-Paul Van Vooren4 and Patrick Stordeur3*

Author Affiliations

1 Department of Dermatology, Erasme University Hospital, 808 Route de Lennick, Brussels, 1070, Belgium

2 Virology, Erasme University Hospital, 808 Route de Lennick, Brussels, 1070, Belgium

3 Immunology, Erasme University Hospital, 808 Route de Lennick, Brussels, 1070, Belgium

4 Internal Medicine, Erasme University Hospital, 808 Route de Lennick, Brussels, 1070, Belgium

5 Department of Infectious Diseases, Saint-Pierre University Hospital, Brussels, 1000, Belgium

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BMC Dermatology 2001, 1:2  doi:10.1186/1471-5945-1-2

Published: 24 July 2001

Abstract

Background

HIV-1 is known to play a critical role in the pathogenesis of AIDS-associated Kaposi's sarcoma (KS). However, it remains controversial whether KS cells are target cells for HIV infection. The aim of this study was to investigate the expression of chemokine receptors in KS cell cultures and to determine whether these cells can be infected by HIV-1.

Material and Methods

KS-derived cells and KS-Y1 cells were investigated using RT-PCR for the expression of CD4, CCR3, CCR5, CCR8 and CXCR4 mRNA. HIV infectivity of these cells was determined by p24 antigen and HIV-1 RNA production, as well as by HIV-1 DNA integration.

Results and Discussion

With the exception of CCR8 which is expressed by KS-derived spindle cell cultures but not by KS-Y1 cells, unstimulated KS cells express no significant levels of CD4, CCR3, CCR5 or CXCR4 mRNA. HIV infectivity assays showed that KS cells were unpermissive to HTLVIIIB and JRFL strains. Although the expression of CXCR4 mRNA could be upregulated by interleukin-1β, stimulation of KS cells by this cytokine did not allow infection by HIV-1.

Conclusions

This shows that KS cells exhibit a chemokine receptor repertoire that does not allow infection by HIV-1. Other cell types making up KS lesions, such as inflammatory cells, are likely to represent the source of HIV-1 products cooperating to promote KS development and progression.