17 results on '"Chomont, Nicolas"'
Search Results
2. Altered memory CCR6+ Th17-polarised T-cell function and biology in people with HIV under successful antiretroviral therapy and HIV elite controllers
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Yero, Alexis, Goulet, Jean-Philippe, Shi, Tao, Costiniuk, Cecilia T., Routy, Jean-Pierre, Tremblay, Cecile, Mboumba Bouassa, Ralph-Sydney, Alexandrova, Yulia, Pagliuzza, Amélie, Chomont, Nicolas, Ancuta, Petronela, and Jenabian, Mohammad-Ali
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- 2024
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3. CD8+ T-cell priming is quantitatively but not qualitatively impaired in people with HIV-1 on antiretroviral therapy
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Cabral-Piccin, Mariela P., Briceño, Olivia, Papagno, Laura, Liouville, Benjamin, White, Eoghann, Perdomo-Celis, Federico, Autaa, Gaëlle, Volant, Stevenn, Llewellyn-Lacey, Sian, Fromentin, Rémi, Chomont, Nicolas, Price, David A., Sáez-Cirión, Asier, Lambotte, Olivier, Katlama, Christine, and Appay, Victor
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- 2024
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4. Isotretinoin promotes elimination of translation-competent HIV latent reservoirs in CD4T cells.
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Howard, J. Natalie, Levinger, Callie, Deletsu, Selase, Fromentin, Rémi, Chomont, Nicolas, and Bosque, Alberto
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IMMUNOLOGIC memory ,ISOTRETINOIN ,HIV-positive persons ,CELL death ,ANTIRETROVIRAL agents - Abstract
Development of novel therapeutic strategies that reactivate latent HIV and sensitize reactivated cells to apoptosis is crucial towards elimination of the latent viral reservoir. Among the clinically relevant latency reversing agents (LRA) under investigation, the γc-cytokine IL-15 and the superagonist N-803 have been shown to reactivate latent HIV ex vivo and in vivo. However, their clinical benefit can be hindered by IL-15 promoting survival of infected cells. We previously identified a small molecule, HODHBt, that sensitizes latently infected cells to death upon reactivation with γc-cytokines through a STAT-dependent pathway. In here, we aimed to identify and evaluate FDA-approved compounds that could also sensitize HIV-infected cells to apoptosis. Using the Connectivity Map (CMap), we identified the retinol derivative 13-cis-retinoic acid (Isotretinoin) causes similar transcriptional changes as HODHBt. Isotretinoin enhances IL-15-mediated latency reversal without inducing proliferation of memory CD4 T cells. Ex vivo analysis of PBMCs from ACTG A5325, where Isotretinoin was administered to ART-suppressed people with HIV, showed that Isotretinoin treatment enhances IL-15-mediated latency reversal. Furthermore, we showed that a combination of IL-15 with Isotretinoin promotes the reduction of translation-competent reservoirs ex vivo. Mechanistically, combination of IL-15 and Isotretinoin increases caspase-3 activation specifically in HIV-infected cells but not uninfected cells. Our results suggest that Isotretinoin can be a novel approach to target and eliminate translation-competent HIV reservoirs. Author summary: Even with the development and rapid advancement of antiretroviral therapies (ART) against HIV in the past three decades, there is still no generalized cure for HIV. Identification of novel therapeutic interventions that target the latent reservoir could provide new avenues to find a cure. In this work, we evaluated the ability of the FDA-approved compound Isotretinoin to reactivate latent HIV and promote a reduction of the latent reservoir ex vivo. Our studies found that Isotretinoin can enhance the ability of IL-15 to reactivate latent reservoirs. Furthermore, using samples from clinical trial ACTG A5325 (NCT01969058) we show that Isotretinoin sensitizes latent HIV to reactivation by IL-15. Finally, we demonstrate that Isotretinoin can sensitize reactivated cells to death via apoptosis. Overall, this study demonstrate that Isotretinoin could be used in combinatorial strategies towards the development of an HIV cure to promote reduction of latent reservoirs. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Similar Viral and Immune Characteristics of Kaposi Sarcoma in ART-treated People Living With HIV and Older Patients With Classic Kaposi Sarcoma.
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Royston, Léna, Jary, Aude, Berini, Carolina A, Mabanga, Tsoarello, Lin, John, Pagliuzza, Amélie, Chomont, Nicolas, Litvinov, Ivan V, Calmy, Alexandra, Leducq, Valentin, Calvez, Vincent, Marcelin, Anne-Geneviève, Isnard, Stéphane, and Routy, Jean-Pierre
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MONONUCLEAR leukocytes ,GRANULOCYTE-colony stimulating factor ,PLATELET-derived growth factor ,HIV ,KAPOSI'S sarcoma - Abstract
Background Reemergence of human herpesvirus 8 (HHV-8)–induced Kaposi sarcoma (KS) in people living with HIV (PLWH) despite antiretroviral therapy (ART) poses a clinical challenge because they already have favorable CD4 T-cell numbers and undetectable viral loads. We observed that clinical presentation in PLWH on ART resembled classic KS found in older HIV-uninfected patients and hypothesized that immunosenescence may thus play a role in occurrence of KS on ART. We compared viral and immune factors implicated in the development of KS in ART-treated PLWH (HIV KS) and HIV-uninfected classic KS patients (cKS), compared to controls without KS (HIV Control, cControls respectively). Methods Plasma, peripheral blood mononuclear cell, and skin tissues were obtained from 11 HIV KS and 11 cKS patients and 2 groups of age-matched controls. Results HIV KS participants were younger than cKS (aged 53 vs 75 years). HHV-8 genotypes did not differ between groups. Despite the younger age and a lower CD4/CD8 ratio, activated, exhausted, and senescent T-cell frequencies were similar between HIV KS and cKS. Anti–HHV-8 immunoglobulin G levels were higher and circulating HHV-8 DNA lower in HIV KS compared with cKS. Circulating platelet-derived growth factors AA-BB and granulocyte colony-stimulating factors were higher in HIV KS We observed similar levels of HHV-8 DNA and PD-1 expression in skin lesions from HIV KS and cKS patients. Conclusions Altogether, early immune senescence could be involved in the development of KS in ART-treated PLWH. Higher anti–HHV-8 immunoglobulin G levels could be linked with lower circulating viral load. Such insights should help developing therapeutical strategies to prevent development and treat KS in PLWH on ART. [ABSTRACT FROM AUTHOR]
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- 2024
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6. Intra-Host Evolution Analyses in an Immunosuppressed Patient Supports SARS-CoV-2 Viral Reservoir Hypothesis
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Fournelle, Dominique, primary, Mostefai, Fatima, additional, Brunet-Ratnasingham, Elsa, additional, Poujol, Raphaël, additional, Grenier, Jean-Christophe, additional, Gálvez, José Héctor, additional, Pagliuzza, Amélie, additional, Levade, Inès, additional, Moreira, Sandrine, additional, Benlarbi, Mehdi, additional, Beaudoin-Bussières, Guillaume, additional, Gendron-Lepage, Gabrielle, additional, Bourassa, Catherine, additional, Tauzin, Alexandra, additional, Grandjean Lapierre, Simon, additional, Chomont, Nicolas, additional, Finzi, Andrés, additional, Kaufmann, Daniel E., additional, Craig, Morgan, additional, and Hussin, Julie G., additional
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- 2024
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7. Metformin Enhances Antibody-Mediated Recognition of HIV-Infected CD4+ T-Cells by Decreasing Viral Release
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Fert, Augustine, primary, Richard, Jonathan, additional, Raymond Marchand, Laurence, additional, Planas, Delphine, additional, Routy, Jean-Pierre, additional, Chomont, Nicolas, additional, Finzi, Andres, additional, and Ancuta, Petronela, additional
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- 2024
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8. IL-32 Drives the Differentiation of Cardiotropic CD4+ T Cells Carrying HIV DNA in People With HIV.
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Ramani, Hardik, Gosselin, Annie, Bunet, Rémi, Jenabian, Mohammad-Ali, Sylla, Mohamed, Pagliuzza, Amélie, Chartrand-Lefebvre, Carl, Routy, Jean-Pierre, Goulet, Jean-Philippe, Thomas, Réjean, Trottier, Benoit, Martel-Laferrière, Valérie, Fortin, Claude, Chomont, Nicolas, Fromentin, Rémi, Landay, Alan L, Durand, Madeleine, Ancuta, Petronela, El-Far, Mohamed, and Tremblay, Cecile
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T cells ,HIV-positive persons ,INTERLEUKIN-32 ,PROTEIN-tyrosine kinases ,IMMUNOLOGIC memory ,VIRAL tropism - Abstract
Interleukin 32 (IL-32) is a potent multi-isoform proinflammatory cytokine, which is upregulated in people with HIV (PWH) and is associated with cardiovascular disease (CVD) risk. However, the impact of IL-32 isoforms on CD4 T-cell cardiotropism, a mechanism potentially contributing to heart inflammation, remains unknown. Here we show that IL-32 isoforms β and γ induce the generation of CCR4
+ CXCR3+ double positive (DP) memory CD4 T-cell subpopulation expressing the tyrosine kinase receptor c-Met, a phenotype associated with heart-homing of T cells. Our ex vivo studies on PWH show that the frequency of DP CD4 T cells is significantly higher in individuals with, compared to individuals without, subclinical atherosclerosis and that DP cells from antiretroviral-naive and treated individuals are highly enriched with HIV DNA. Together, these data demonstrate that IL-32 isoforms have the potential to induce heart-homing of HIV-infected CD4 T cells, which may further aggravate heart inflammation and CVD in PWH. [ABSTRACT FROM AUTHOR]- Published
- 2024
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9. Measuring Human Immunodeficiency Virus Reservoirs: Do We Need to Choose Between Quantity and Quality?
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Roux, Hélène and Chomont, Nicolas
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The persistence of latent viral genomes in people receiving antiretroviral therapy (ART) is the main obstacle to a cure for human immunodeficiency virus (HIV) infection. Viral reservoirs can be defined as cells harboring HIV genomes that have the ability to produce infectious virions. Precise quantification of the cellular reservoirs of HIV is challenging because these cells are rare, heterogeneous, and outnumbered by a larger number of cells carrying defective genomes. In addition, measuring the inducibility of these proviruses requires functional assays and remains technically difficult. The recent development of single-cell and single-viral genome approaches revealed additional layers of complexity: the cell subsets that harbor proviruses are heterogeneous and their ability to be induced is variable. A substantial fraction of intact HIV genomes may be permanently silenced after years of ART, revealing the underappreciated importance of induction assays. As such, a simple approach that would assess simultaneously the genetic intactness and the inducibility of the reservoir is still lacking. In this study, we review recent advances in the development of methods to quantify and characterize persistently infected cells, and we discuss how these findings can inform the design of future assays aimed at measuring the size of the intact and inducible HIV reservoir. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Plasma Human Immunodeficiency Virus 1 Soluble Glycoprotein 120 Association With Correlates of Immune Dysfunction and Inflammation in Antiretroviral Therapy–Treated Individuals With Undetectable Viremia.
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Benlarbi, Mehdi, Richard, Jonathan, Bourassa, Catherine, Tolbert, William D, Chartrand-Lefebvre, Carl, Gendron-Lepage, Gabrielle, Sylla, Mohamed, El-Far, Mohamed, Messier-Peet, Marc, Guertin, Camille, Turcotte, Isabelle, Fromentin, Rémi, Verly, Myriam Maude, Prévost, Jérémie, Clark, Andrew, Mothes, Walther, Kaufmann, Daniel E, Maldarelli, Frank, Chomont, Nicolas, and Bégin, Philippe
- Abstract
Background Chronic inflammation persists in some people living with human immunodeficiency virus (HIV) during antiretroviral therapy and is associated with premature aging. The glycoprotein 120 (gp120) subunit of HIV-1 envelope sheds and can be detected in plasma, showing immunomodulatory properties even in the absence of detectable viremia. We evaluated whether plasma soluble gp120 (sgp120) and a family of gp120-specific anti–cluster A antibodies, linked to CD4 depletion in vitro, contribute to chronic inflammation, immune dysfunction, and subclinical cardiovascular disease in participants of the Canadian HIV and Aging Cohort Study with undetectable viremia. Methods Cross-sectional assessment of sgp120 and anti–cluster A antibodies was performed in 386 individuals from the cohort. Their association with proinflammatory cytokines and subclinical coronary artery disease was assessed using linear regression models. Results High levels of sgp120 and anti–cluster A antibodies were inversely correlated with CD4
+ T cell count and CD4/CD8 ratio. The presence of sgp120 was associated with increased levels of interleukin 6. In participants with detectable atherosclerotic plaque and detectable sgp120, anti–cluster A antibodies and their combination with sgp120 levels correlated positively with the total volume of atherosclerotic plaques. Conclusions This study showed that sgp120 may act as a pan toxin causing immune dysfunction and sustained inflammation in a subset of people living with HIV, contributing to the development of premature comorbid conditions. [ABSTRACT FROM AUTHOR]- Published
- 2024
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11. CD8+ T-cell priming is quantitatively but not qualitatively impaired in people with HIV-1 on antiretroviral therapy.
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Cabral-Piccin, Mariela P., Briceño, Olivia, Papagno, Laura, Liouville, Benjamin, White, Eoghann, Perdomo-Celis, Federico, Autaa, Gaëlle, Volant, Stevenn, Llewellyn-Lacey, Sian, Fromentin, Rémi, Chomont, Nicolas, Price, David A., Sáez-Cirión, Asier, Lambotte, Olivier, Katlama, Christine, and Appay, Victor
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- 2024
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12. Transmission of highly virulent CXCR4 tropic HIV-1 through the mucosal route in an individual with a wild-type CCR5 genotype.
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Marichannegowda MH, Setua S, Bose M, Sanders-Buell E, King D, Zemil M, Wieczorek L, Diaz-Mendez F, Chomont N, Thomas R, Francisco L, Eller LA, Polonis VR, Tovanabutra S, Heredia A, Tagaya Y, Michael NL, Robb ML, and Song H
- Abstract
Background: Nearly all transmitted/founder (T/F) HIV-1 are CCR5 (R5)-tropic. While previous evidence suggested that CXCR4 (X4)-tropic HIV-1 are transmissible, virus detection and characterization were not at the earliest stages of acute infection., Methods: We identified an X4-tropic T/F HIV-1 in a participant (40700) in the RV217 acute infection cohort. Coreceptor usage was determined in TZM-bl cell line, NP-2 cell lines, and primary CD4
+ T cells using pseudovirus and infectious molecular clones. CD4 subset dynamics were analyzed using flow cytometry. Viral load in each CD4 subset was quantified using cell-associated HIV RNA assay and total and integrated HIV DNA assay., Findings: Participant 40700 was infected by an X4 tropic HIV-1 without CCR5 using ability. This participant experienced significantly faster CD4 depletion compared to R5 virus infected individuals in the same cohort. Naïve and central memory (CM) CD4 subsets declined faster than effector memory (EM) and transitional memory (TM) subsets. All CD4 subsets, including the naïve, were productively infected. Increased CD4+ T cell activation was observed over time. This X4-tropic T/F virus is resistant to broadly neutralizing antibodies (bNAbs) targeting V1/V2 and V3 regions, while most of the R5 T/F viruses in the same cohort are sensitive to the same panel of bNAbs., Interpretation: X4-tropic HIV-1 is transmissible through mucosal route in people with wild-type CCR5 genotype. The CD4 subset tropism of HIV-1 may be an important determinant for HIV-1 transmissibility and virulence., Funding: Institute of Human Virology, National Institutes of Health, Henry M. Jackson Foundation for the Advancement of Military Medicine., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)- Published
- 2024
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13. Sustained IFN signaling is associated with delayed development of SARS-CoV-2-specific immunity.
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Brunet-Ratnasingham E, Morin S, Randolph HE, Labrecque M, Bélair J, Lima-Barbosa R, Pagliuzza A, Marchitto L, Hultström M, Niessl J, Cloutier R, Sreng Flores AM, Brassard N, Benlarbi M, Prévost J, Ding S, Anand SP, Sannier G, Marks A, Wågsäter D, Bareke E, Zeberg H, Lipcsey M, Frithiof R, Larsson A, Zhou S, Nakanishi T, Morrison D, Vezina D, Bourassa C, Gendron-Lepage G, Medjahed H, Point F, Richard J, Larochelle C, Prat A, Cunningham JL, Arbour N, Durand M, Richards JB, Moon K, Chomont N, Finzi A, Tétreault M, Barreiro L, Wolf G, and Kaufmann DE
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- Humans, Female, Male, Middle Aged, Immunoglobulin G blood, Immunoglobulin G immunology, CD4-Positive T-Lymphocytes immunology, Aged, Adult, Spike Glycoprotein, Coronavirus immunology, Spike Glycoprotein, Coronavirus metabolism, Spike Glycoprotein, Coronavirus genetics, COVID-19 immunology, SARS-CoV-2 immunology, Antibodies, Viral immunology, Antibodies, Viral blood, Signal Transduction immunology, Interferons metabolism, Interferons immunology
- Abstract
Plasma RNAemia, delayed antibody responses and inflammation predict COVID-19 outcomes, but the mechanisms underlying these immunovirological patterns are poorly understood. We profile 782 longitudinal plasma samples from 318 hospitalized patients with COVID-19. Integrated analysis using k-means reveals four patient clusters in a discovery cohort: mechanically ventilated critically-ill cases are subdivided into good prognosis and high-fatality clusters (reproduced in a validation cohort), while non-critical survivors segregate into high and low early antibody responders. Only the high-fatality cluster is enriched for transcriptomic signatures associated with COVID-19 severity, and each cluster has distinct RBD-specific antibody elicitation kinetics. Both critical and non-critical clusters with delayed antibody responses exhibit sustained IFN signatures, which negatively correlate with contemporaneous RBD-specific IgG levels and absolute SARS-CoV-2-specific B and CD4
+ T cell frequencies. These data suggest that the "Interferon paradox" previously described in murine LCMV models is operative in COVID-19, with excessive IFN signaling delaying development of adaptive virus-specific immunity., (© 2024. The Author(s).)- Published
- 2024
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14. IL-32 Drives the Differentiation of Cardiotropic CD4+ T Cells Carrying HIV DNA in People With HIV.
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Ramani H, Gosselin A, Bunet R, Jenabian MA, Sylla M, Pagliuzza A, Chartrand-Lefebvre C, Routy JP, Goulet JP, Thomas R, Trottier B, Martel-Laferrière V, Fortin C, Chomont N, Fromentin R, Landay AL, Durand M, Ancuta P, El-Far M, and Tremblay C
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- Female, Humans, Male, Cell Differentiation, DNA, Viral, HIV-1, Protein Isoforms genetics, Protein Isoforms metabolism, CD4-Positive T-Lymphocytes immunology, HIV Infections immunology, HIV Infections virology, Interleukins metabolism, Interleukins genetics
- Abstract
Interleukin 32 (IL-32) is a potent multi-isoform proinflammatory cytokine, which is upregulated in people with HIV (PWH) and is associated with cardiovascular disease (CVD) risk. However, the impact of IL-32 isoforms on CD4 T-cell cardiotropism, a mechanism potentially contributing to heart inflammation, remains unknown. Here we show that IL-32 isoforms β and γ induce the generation of CCR4+CXCR3+ double positive (DP) memory CD4 T-cell subpopulation expressing the tyrosine kinase receptor c-Met, a phenotype associated with heart-homing of T cells. Our ex vivo studies on PWH show that the frequency of DP CD4 T cells is significantly higher in individuals with, compared to individuals without, subclinical atherosclerosis and that DP cells from antiretroviral-naive and treated individuals are highly enriched with HIV DNA. Together, these data demonstrate that IL-32 isoforms have the potential to induce heart-homing of HIV-infected CD4 T cells, which may further aggravate heart inflammation and CVD in PWH., Competing Interests: Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
- Published
- 2024
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15. Metformin Enhances Antibody-Mediated Recognition of HIV-Infected CD4 + T-Cells by Decreasing Viral Release.
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Fert A, Richard J, Marchand LR, Planas D, Routy JP, Chomont N, Finzi A, and Ancuta P
- Abstract
The mechanistic target of rapamycin (mTOR) positively regulates multiple steps of the HIV-1 replication cycle. We previously reported that a 12-weeks supplementation of antiretroviral therapy (ART) with metformin, an indirect mTOR inhibitor used in type-2 diabetes treatment, reduced mTOR activation and HIV transcription in colon-infiltrating CD4
+ T-cells, together with systemic inflammation in nondiabetic people with HIV-1 (PWH). Herein, we investigated the antiviral mechanisms of metformin. In a viral outgrowth assay performed with CD4+ T-cells from ART-treated PWH, and upon infection in vitro with replication-competent and VSV-G-pseudotyped HIV-1, metformin decreased virion release, but increased the frequency of productively infected CD4low HIV-p24+ T-cells. These observations coincided with increased BST2/Tetherin (HIV release inhibitor) and Bcl-2 (pro-survival factor) expression, and improved recognition of productively infected T-cells by HIV-1 Envelope antibodies. Thus, metformin exerts pleiotropic effects on post-transcription/translation steps of the HIV-1 replication cycle and may be used to accelerate viral reservoir decay in ART-treated PWH., Competing Interests: CONFLICT OF INTEREST The authors declare no competing interests.- Published
- 2024
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16. CD8 + T-cell priming is quantitatively but not qualitatively impaired in people with HIV-1 on antiretroviral therapy.
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Cabral-Piccin MP, Briceño O, Papagno L, Liouville B, White E, Perdomo-Celis F, Autaa G, Volant S, Llewellyn-Lacey S, Fromentin R, Chomont N, Price DA, Sáez-Cirión A, Lambotte O, Katlama C, and Appay V
- Subjects
- Humans, CD8-Positive T-Lymphocytes, HIV Infections drug therapy, HIV-1, HIV Seropositivity
- Abstract
Background: The induction of de novo CD8 + T-cell responses is essential for protective antiviral immunity, but this process is often impaired in people with HIV-1 (PWH). We investigated the extent to which the immune competence of naive CD8 + T cells, a key determinant of priming efficacy, could be preserved or restored in PWH via long-term antiretroviral therapy (ART)., Methods: We used flow cytometry, molecular analyses of gene transcription and telomere length, and a fully validated priming assay to characterize naive CD8 + T cells ex vivo and evaluate the induction of antigen-specific effector/memory CD8 + T cells in vitro , comparing age-matched healthy uninfected donors (HUDs), PWH on ART, and natural HIV-1 controllers (HICs)., Results: We found that naive CD8 + T cells were numerically reduced and exhibited a trend toward shorter telomere lengths in PWH on ART compared with HUDs and HICs. These features associated with impaired priming efficacy. However, we also found that naive CD8 + T cells were fully equipped proliferatively and transcriptionally in PWH on ART, enabling the generation of antigen-specific effector/memory CD8 + T cells with functional and phenotypic attributes comparable to those primed from HUDs., Conclusion: Our data suggest that naive CD8 + T cells in PWH on ART are intrinsically capable of generating functionally and phenotypically intact effector/memory CD8 + T cells in response to antigen, despite evidence of senescence and an overall numerical reduction that compromises priming efficacy relative to HUDs and HICs., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)
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- 2024
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17. Gaining Biological Insights through Supervised Data Visualization.
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Rhodes JS, Aumon A, Morin S, Girard M, Larochelle C, Brunet-Ratnasingham E, Pagliuzza A, Marchitto L, Zhang W, Cutler A, Grand'Maison F, Zhou A, Finzi A, Chomont N, Kaufmann DE, Zandee S, Prat A, Wolf G, and Moon KR
- Abstract
Dimensionality reduction-based data visualization is pivotal in comprehending complex biological data. The most common methods, such as PHATE, t-SNE, and UMAP, are unsupervised and therefore reflect the dominant structure in the data, which may be independent of expert-provided labels. Here we introduce a supervised data visualization method called RF-PHATE, which integrates expert knowledge for further exploration of the data. RF-PHATE leverages random forests to capture intricate featurelabel relationships. Extracting information from the forest, RF-PHATE generates low-dimensional visualizations that highlight relevant data relationships while disregarding extraneous features. This approach scales to large datasets and applies to classification and regression. We illustrate RF-PHATE's prowess through three case studies. In a multiple sclerosis study using longitudinal clinical and imaging data, RF-PHATE unveils a sub-group of patients with non-benign relapsingremitting Multiple Sclerosis, demonstrating its aptitude for time-series data. In the context of Raman spectral data, RF-PHATE effectively showcases the impact of antioxidants on diesel exhaust-exposed lung cells, highlighting its proficiency in noisy environments. Furthermore, RF-PHATE aligns established geometric structures with COVID-19 patient outcomes, enriching interpretability in a hierarchical manner. RF-PHATE bridges expert insights and visualizations, promising knowledge generation. Its adaptability, scalability, and noise tolerance underscore its potential for widespread adoption.
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- 2024
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