Cited by 44HIV Research and TreatmentHIV-related health complications and treatmentsChemokine receptors and signaling

The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.

Monocytes Contribute to Differential Immune Pressure on R5 versus X4 HIV through the Adipocytokine Visfatin/NAMPT

Open access
Van den Bergh, Rafael, Morin, Sébastien, Sass, Hans Jürgen, Grzesiek, Stephan, Vekemans, Marc, Florence, Eric, Thanh Thi Tran, Huyen, Imiru, Rosina Gabriel, Heyndrickx, Leo, Vanham, Guido, De Baetselier, Patrick, Raes, Geert·2012·PLoS ONE

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.

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Crossref · 10.1371/journal.pone.0035074

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  • Pretreatment of macrophages with CCR5 and TLR4 blockers partially alleviates rhNAMPT-induced M2 polarization in macrophages.

    “In line with previous reports 70, 71, we pretreated macrophages with C-C chemokine receptor type 5 (CCR5) and Toll-like receptor 4 (TLR4) blockers, which indeed partially alleviated rhNAMPT-induced M2 polarization in macrophages (Figure S7).”

    From Nicotinamide phosphoribosyltransferase prompts bleomycin-induced pulmonary fibrosis by driving macrophage M2 polarization in mice (2024) · cites this paper as [70]

    The Results section (‘Visfatin Interacts Directly with the CCR5 Coreceptor’; page unavailable) reports a specific interaction between visfatin/NAMPT and CCR5, supporting the rationale for testing a CCR5 blocker. It does not report pretreatment with CCR5 or TLR4 blockers or an effect on M2 polarization. The citing sentence presents the partial alleviation as its own Figure S7 result, not as a result of this source. (LLM, conf=0.84)

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Research works printed but not linked: 1

  1. LJ Reed, 1938, A simple method of estimating fifty percent endpoints., Am J Hyg, 27, 493

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Metadata

Authors
Van den Bergh, R., Morin, S., Sass, H. J., Grzesiek, S., Vekemans, M., Florence, E., Thanh Thi Tran, H., Imiru, R. G., Heyndrickx, L., Vanham, G., De Baetselier, P., & Raes, G.
Affiliations
  • University of Basel (CH)
  • Instituut voor Tropische Geneeskunde (BE)
  • Vrije Universiteit Brussel (BE)
Venue
PLoS ONE
Published
2012-04-06
Volume
7
Issue
4
Pages
e35074
ISSN
1932-6203 (ISSN-L)
OpenAlex
W2091304953
Cited by
40
References
46
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 1 · 2015: 1 · 2014: 2
FWCI
0.43
Type
journal article
Language
en
Open access
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • European Molecular Biology Organization
  • Vlaamse regering
Topics
  • Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
  • Health Sciences › Medicine › Infectious Diseases › HIV-related health complications and treatments
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords
visfatin, monocytes, CCR5, CXCR4, viral fitness, viral competition, macrophages, HIV tropism, adipokines
MeSH terms
Cells, Cultured, HIV, Humans, Immunity, Innate, Monocytes, Selection, Genetic, Species Specificity, Virus Replication, HIV Infections, Receptors, CCR5, Receptors, CXCR4, Surface Plasmon Resonance, Nicotinamide Phosphoribosyltransferase, Host-Pathogen Interactions

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