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Monocytes contribute to differential immune pressure on R5 versus X4 HIV through the adipocytokine Visfatin/NAMPT

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dc.contributor.author Van den Bergh, R.
dc.contributor.author Morin, S.
dc.contributor.author Sass, H. J.
dc.contributor.author Grzesiek, S.
dc.contributor.author Vekemans, M.
dc.contributor.author Florence, E.
dc.contributor.author Than, H. T. T.
dc.contributor.author Imiru, R. G.
dc.contributor.author Heyndrickx, L.
dc.contributor.author Vanham, G.
dc.contributor.author De Baetselier, P.
dc.contributor.author Raes, G.
dc.date.accessioned 2012-04-26T13:45:22Z
dc.date.available 2012-04-26T13:45:22Z
dc.date.issued 2012
dc.identifier.issn 1932-6203
dc.identifier.doi http://dx.doi.org/10.1371/journal.pone.0035074
dc.identifier.other ITG-C5A
dc.identifier.other ITG-C6A
dc.identifier.other ITG-B9A
dc.identifier.other ITG-B10A
dc.identifier.other MULTI
dc.identifier.other DCS
dc.identifier.other U-STDCLI
dc.identifier.other U-TRAVC
dc.identifier.other DBM
dc.identifier.other U-VIROL
dc.identifier.other JIF
dc.identifier.other DOI
dc.identifier.other Abstract
dc.identifier.other UPD45
dc.identifier.other FTA
dc.identifier.uri http://hdl.handle.net/10390/6973
dc.description.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. en
dc.language English en
dc.subject Viral diseases en
dc.subject HIV en
dc.subject AIDS en
dc.subject Immune response en
dc.subject Inhibition en
dc.subject Strains en
dc.subject Infectivity en
dc.subject Monocytes en
dc.subject Visfatin en
dc.subject CCR5-receptor antagonists en
dc.subject CXCR4 en
dc.subject P24 en
dc.subject Viral fitness en
dc.subject Mathematical modeling en
dc.subject In vivo en
dc.subject Laboratory techniques and procedures en
dc.title Monocytes contribute to differential immune pressure on R5 versus X4 HIV through the adipocytokine Visfatin/NAMPT en
dc.type Article-E en
dc.citation.issue 4 en
dc.citation.jtitle PLoS ONE en
dc.citation.volume 7 en
dc.citation.pages e35074 en
dc.identifier.pmid http://www.ncbi.nlm.nih.gov/pubmed/22493731
dc.citation.jabbreviation PLoS ONE en


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