HIV-1 virus strains use the chemokine receptors, CCR-5, CXCR-4, or both, to enter cells (reviewed in reference 1). Expression of these chemokine receptors may predetermine susceptibility of hematopoietic subsets to HIV-1 infection. Certain cytokines can influence the dynamics of HIV-1 infection by altering chemokine receptor expression levels on hematopoietic cells.

During chronic HIV-1 infection, proinflammatory cytokines such as TNF-alpha and IFN-gamma are secreted in excess.^2,3 IFN-gamma increases cell surface expression of CCR-5 by human mononuclear phagocytes⁴ and of CXCR-4 by primary hematopoietic cells.⁵ In addition, GM-CSF can decrease⁶ and IL-10 can increase expression of CCR-5.⁷ Further research into cytokine-mediated regulation of chemokine receptors may lead to increased understanding of how these receptors affect the pathogenesis of AIDS.

References

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