A look at HIV journey

Blanchet, Fabien P.; Moris, Arnaud; Mitchell, John P.; Piguet, Vincent

doi:10.1097/coh.0b013e328349b0a0

Cited by 23 publications

(9 citation statements)

References 61 publications

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“…CXCR6 is also involved in the formation of the immunological synapse upon interaction with its ligand CXCL16, a membrane-bound chemokine expressed by DC [62,93]. This interaction my lead to efficient transmission of HIV within the virological synapse [94]. CXCL16 is also expressed by CD16 + monocytes [95].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies Peroxisome Proliferator-Activated Receptor Gammaas an intrinsic negative regulator of viral replication

et al. 2013

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BackgroundWe previously demonstrated that primary Th1Th17 cells are highly permissive to HIV-1, whereas Th1 cells are relatively resistant. Molecular mechanisms underlying these differences remain unknown.ResultsExposure to replication competent and single-round VSV-G pseudotyped HIV strains provide evidence that superior HIV replication in Th1Th17 vs. Th1 cells was regulated by mechanisms located at entry and post-entry levels. Genome-wide transcriptional profiling identified transcripts upregulated (n = 264) and downregulated (n = 235) in Th1Th17 vs. Th1 cells (p-value < 0.05; fold change cut-off 1.3). Gene Set Enrichment Analysis revealed pathways enriched in Th1Th17 (nuclear receptors, trafficking, p38/MAPK, NF-κB, p53/Ras, IL-23) vs. Th1 cells (proteasome, interferon α/β). Differentially expressed genes were classified into biological categories using Gene Ontology. Th1Th17 cells expressed typical Th17 markers (IL-17A/F, IL-22, CCL20, RORC, IL-26, IL-23R, CCR6) and transcripts functionally linked to regulating cell trafficking (CEACAM1, MCAM), activation (CD28, CD40LG, TNFSF13B, TNFSF25, PTPN13, MAP3K4, LTB, CTSH), transcription (PPARγ, RUNX1, ATF5, ARNTL), apoptosis (FASLG), and HIV infection (CXCR6, FURIN). Differential expression of CXCR6, PPARγ, ARNTL, PTPN13, MAP3K4, CTSH, SERPINB6, PTK2, and ISG20 was validated by RT-PCR, flow cytometry and/or confocal microscopy. The nuclear receptor PPARγ was preferentially expressed by Th1Th17 cells. PPARγ RNA interference significantly increased HIV replication at levels post-entry and prior HIV-DNA integration. Finally, the activation of PPARγ pathway via the agonist Rosiglitazone induced the nuclear translocation of PPARγ and a robust inhibition of viral replication.ConclusionsThus, transcriptional profiling in Th1Th17 vs. Th1 cells demonstrated that HIV permissiveness is associated with a superior state of cellular activation and limited antiviral properties and identified PPARγ as an intrinsic negative regulator of viral replication. Therefore, triggering PPARγ pathway via non-toxic agonists may contribute to limiting covert HIV replication and disease progression during antiretroviral treatment.

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Section: Discussionmentioning

confidence: 99%

Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies Peroxisome Proliferator-Activated Receptor Gammaas an intrinsic negative regulator of viral replication

et al. 2013

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“…DCs are involved in maintaining a balance between tolerance versus protective immunity at both the innate and adaptive levels, which process is pivotal at mucosal sites, where immune homeostasis processes warrant peripheral integrity, and where the main battle with HIV takes place [1–4]. Recent studies have demonstrated the importance of cross-talk between epithelial cells and mDC populations in maintenance of a homeostatic balance of regulatory versus inflammatory responses at the mucosal level [73–75].…”

Section: The Importance Of Dcs At Mucosal Sitesmentioning

confidence: 99%

“…There, DCs are one of the earliest cell types to be exposed to the virus and present an inherent capacity to orchestrate a homeostatic balance between tolerance and protection [1–4]. It is likely that the incapacity to keep a balance in these homeostatic processes will promote inflammation and lead to disease progression [5].…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, the capacity to maintain immune homeostasis at mucosal sites will probably allow for better control of HIV-infection. The general effects of HIV-infection and disease on DC populations have been recently reviewed [1–4] and are beyond the scope of this work. This perspective review will focus on the potential impact of DCs on HIV-related B-cell disorders and responses.…”

Section: Introductionmentioning

confidence: 99%

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Influence of Dendritic Cells on B-Cell Responses during HIV Infection

Poudrier

Chagnon-Choquet

Roger

2012

Clinical and Developmental Immunology

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Dendritic cells (DCs) modulate B-cell differentiation, activation, and survival mainly through production of growth factors such as B lymphocyte stimulator (BLyS/BAFF). DC populations have been reported to be affected in number, phenotype and function during HIV infection and such alterations may contribute to the dysregulation of the B-cell compartment. Herein, we reflect on the potential impact of DC on the pathogenesis of HIV-related B cell disorders, and how DC status may modulate the outcome of mucosal B cell responses against HIV, which are pivotal to the control of disease. A concept that could be extrapolated to the overall outcome of HIV disease, whereby control versus progression may reside in the host’s capacity to maintain DC homeostasis at mucosal sites, where DC populations present an inherent capacity of modulating the balance between tolerance and protection, and are amongst the earliest cell types to be exposed to the virus.

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“…Furthermore, application of this technique would open possibilities for a more detailed investigation of HIV-1 cell‑to-cell transmission in 3d tissue cultures. In in vivo systems, directed virus release and transmission through direct contacts between infected cell and uninfected cells (so-called virological synapses) represents an effective pathway of HIV-1 transmission (for reviews see [101,102,103,104]). However, quantitative kinetic analyses of HIV-1 budding site formation have so far been limited to TIRF microscopy, which cannot visualize intracellular synapses, and were restricted to flat adherent model cell lines instead of the physiological target cells.…”

Section: Future Directionsmentioning

confidence: 99%

Quantitative Live-Cell Imaging of Human Immunodeficiency Virus (HIV-1) Assembly

Baumgärtel

Müller

Lamb

2012

Viruses

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Advances in fluorescence methodologies make it possible to investigate biological systems in unprecedented detail. Over the last few years, quantitative live-cell imaging has increasingly been used to study the dynamic interactions of viruses with cells and is expected to become even more indispensable in the future. Here, we describe different fluorescence labeling strategies that have been used to label HIV-1 for live cell imaging and the fluorescence based methods used to visualize individual aspects of virus-cell interactions. This review presents an overview of experimental methods and recent experiments that have employed quantitative microscopy in order to elucidate the dynamics of late stages in the HIV-1 replication cycle. This includes cytosolic interactions of the main structural protein, Gag, with itself and the viral RNA genome, the recruitment of Gag and RNA to the plasma membrane, virion assembly at the membrane and the recruitment of cellular proteins involved in HIV-1 release to the nascent budding site.

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A look at HIV journey

Abstract: It is becoming evident that a better characterization of the early events of HIV transmission and the involvement of dendritic cell subtypes in this process would contribute to strengthen our efforts to improve the current therapeutic and prophylactic strategies.

Cited by 23 publications

References 61 publications

Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies Peroxisome Proliferator-Activated Receptor Gammaas an intrinsic negative regulator of viral replication

Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies Peroxisome Proliferator-Activated Receptor Gammaas an intrinsic negative regulator of viral replication

Influence of Dendritic Cells on B-Cell Responses during HIV Infection

Quantitative Live-Cell Imaging of Human Immunodeficiency Virus (HIV-1) Assembly

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