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Monocytes contribute to differential immune pressure on R5 versus X4 HIV through the adipocytokine visfatin/NAMPT
Authors:Van den Bergh Rafael  Morin Sébastien  Sass Hans Jürgen  Grzesiek Stephan  Vekemans Marc  Florence Eric  Tran Huyen Thanh Thi  Imiru Rosina Gabriel  Heyndrickx Leo  Vanham Guido  De Baetselier Patrick  Raes Geert
Institution:Department of Molecular and Cellular Interactions, VIB, Brussels, Belgium. rvdbergh@vub.ac.be
Abstract:

Background

The immune system exerts a diversifying selection pressure on HIV through cellular, humoral and innate mechanisms. This pressure drives viral evolution throughout infection. A better understanding of the natural immune pressure on the virus during infection is warranted, given the clinical interest in eliciting and sustaining an immune response to HIV which can help to control the infection. We undertook to evaluate the potential of the novel HIV-induced, monocyte-derived factor visfatin to modulate viral infection, as part of the innate immune pressure on viral populations.

Results

We show that visfatin is capable of selectively inhibiting infection by R5 HIV strains in macrophages and resting PBMC in vitro, while at the same time remaining indifferent to or even favouring infection by X4 strains. Furthermore, visfatin exerts a direct effect on the relative fitness of R5 versus X4 infections in a viral competition setup. Direct interaction of visfatin with the CCR5 receptor is proposed as a putative mechanism for this differential effect. Possible in vivo relevance of visfatin induction is illustrated by its association with the dominance of CXCR4-using HIV in the plasma.

Conclusions

As an innate factor produced by monocytes, visfatin is capable of inhibiting infections by R5 but not X4 strains, reflecting a potential selective pressure against R5 viruses.
Keywords:
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