15th International AIDS Conference Bangkok, Thailand - July 11-16, 2004

Int Conf AIDS 2004 Jul 11-16; 15:(abstract no. MoOrA1047)

Schmidt RE, Ansari AW, Heiken H
Dept. of Clinical Immunology, Hannover Medical School, Hannover, Germany

BACKGROUND: HIV-1, in most instances modulates the host cellular environment by altering the cytokine and chemokine network. A series of inflammatory chemokines including the [beta chemokine MCP-1/CCL2 is induced during viral infections. Some of these mediators regulate the viral replication and CCL2 is reported as one of them. Our group is interested to investigate the impact of HIV-1 viremia on CCL2 gene regulaion.

METHODS: RNA was isolated from PBMCs from HIV-1 viremic and aviremic individuals (n=5). Gene expression profiling was carried out by DNA microarray on pooled RNA samples. Array results were further verified by quantitative real-time PCR. In order to correlate the mRNA expression with protein levels, CCL2 ELISA was performed on serum samples derived from HIV-1 viremic and aviremic patients (n=18) as well as healthy donors as controls. The majority of patients were treated with HAART.

RESULTS: Microarray gene expression profile of HIV-1 viremic individuals showed a marked increase in the host inflammatory chemokine/cytokine gene expression in general. There was a several fold change in C-C chemokine MCP-1/CCL2, C-X-C chemokine CXC10 and IFN-γ in viremic as compared to aviremic patients. The quantitative real-time PCR analysis showed similar patterns in the above inflammatory mediators. A significantly higher level (P=0.0008) of CCL2 production was observed in serum of HIV-1 viremic as compared to aviremic and healthy controls. Conclusion The comparative gene expression profiling reveals an upregulation in the transcripts of several inflammatory chemokine/cytokine genes in HIV-1 viremic individuals. Interestingly, the increase in chemokine CCL2 gene expression is more pronounced in HIV-1 viremic as compared to aviremic patients. Moreover, HIV-1 viremic patient also showed an elevated CCL2 production in their plasma. These results suggest that HIV-1 viremia differentially regulates the CCL2 gene expression in HIV-1 infected individuals. Supported by DFG SFB566/A02

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MoOrA1047

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