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Do monocytes use the novel adipocytokine Visfatin/NAMPT/PBEF1 to flip the HIV coreceptor switch?

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The Human Immunodeficiency Virus (HIV) coreceptor switch, which entails the change in preferential coreceptor usage of the virus for CCR5 to CXCR4 in ~50% of all HIV subtype B infected patients, is an important determinant in the pathogenesis of HIV infection. However, the mechanisms underlying this switch are poorly understood, and prognostic markers for this switch are unknown. Here, we describe the upregulation of the novel adipocytokine visfatin (NAMPT) in monocytes of therapy-naïve HIV patients, which is reversed during antiretroviral therapy. Induction of visfatin was observed both at the mRNA and protein level and was mirrored by an increase in plasma visfatin in therapy-naïve HIV patients. Visfatin expression correlates with the viral load, and high visfatin expression appears to be associated with the dominance of CXCR4-using HIV in the plasma. We show that visfatin is capable of selectively reducing the infectivity of CCR5-using clones in primary cells (macrophages, resting PBMC) in vitro, while at the same time remaining indifferent to or even favouring infection by CXCR4-using virus. As such, visfatin may play an important contributing role in the development of the HIV coreceptor switch by mounting a selective pressure against CCR5-using and in favour of CXCR4-using viruses.

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Correspondence to Rafael Van den Bergh.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Keywords

  • Human Immunodeficiency Virus
  • Protein Level
  • Viral Load
  • Important Determinant
  • Selective Pressure