Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
UNKNOWN
Total Enrollment
240 participants
Study Classification
OBSERVATIONAL
Study Start Date
2020-04-17
Study Completion Date
2025-03-31
Brief Summary
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The investigators propose that the lack of immune response in InR is driven by HIV-containing platelets that might interact with macrophages and CD4+ T-cells although by different mechanisms. In the one hand, HIV-sheltering platelets might fuel tissue HIV macrophage and in turn T cell reservoirs as observed in InRs and/or maintain a low-level viral replication in macrophages, sustaining a persistent inflammatory profile on in these cells. In the other hand,HIV-sheltering platelets might induce CD4+ T-cells dysfunctions via platelets/ectosomes, although without promoting platelet-to-T-cell HIV transfer/infection, thereby increasing the number of peripheral inflammatory TH17 cells and a TH17/Treg unbalance as observed in InRs.
Main Objectives:
i) To characterize and the molecular and functional level the platelet factors implicated in HIV transfer to tissue-like macrophages as well as in the immunomodulatory activity of HIV-containing platelets on macrophages and CD4+ T-cells.
ii) To interrogate the transfer of HIV-containing platelet-derived mRNA and microRNA to tissue-like macrophages and CD4+ T-cells as one major mechanism of target cell immunomodulation.
iii) To investigate the therapeutic potential of anti-platelet aggregation/activation agents (e.g. Abciximab), known to block platelet-immune cell interaction, in improving immune cell functions in vitro and promoting immunological recovery in vivo.
Main Objectives:
i) To characterize and the molecular and functional level the platelet factors implicated in HIV transfer to tissue-like macrophages as well as in the immunomodulatory activity of HIV-containing platelets on macrophages and CD4+ T-cells.
ii) To interrogate the transfer of HIV-containing platelet-derived mRNA and microRNA to tissue-like macrophages and CD4+ T-cells as one major mechanism of target cell immunomodulation.
iii) To investigate the therapeutic potential of anti-platelet aggregation/activation agents (e.g. Abciximab), known to block platelet-immune cell interaction, in improving immune cell functions in vitro and promoting immunological recovery in vivo.
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Detailed Description
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The investigators have recently shown that infectious HIV is carried by platelets in the blood of HIV-infected patients which failed to respond immunologically to cART despite viral suppression (Immunological nonresponders, InRs) and that platelets can mediate HIV transmission to macrophages in vitro, in line with our recent description of HIV reservoir occurrence and establishment in macrophages in cART-suppressed patients. Around 20% of the overall cART-treated patients are InRs that fail to reconstitute their competent immune status despite treatment observance with prolonged viral suppression. The causes of this immunological failure remain unclear and no treatment is available to improve the health of InRs, which are at higher risk of AIDS and non-AIDS morbidity and mortality. The poor immunological recovery in InRs is mainly driven by a sustained low CD4+ T-cell counts that relies on persistent inflammation and immune activation affecting T-cell population profile.
Platelets are cleared by tissue macrophages in vivo in physiological or inflammatory contexts, what could represent a route for HIV to establish reservoirs in macrophages. We have shown that HIV sheltered in platelets can transfer infection to macrophages, in a process blocked by anti-αIIb/ β3 antibody Abciximab. This infection is productive as in turn, infection spreads replication-competent virus to non-infected CD4+ T-cells. This viral spread may increase the blood T-cell HIV reservoir, a hallmark of immunological failure as observed in InRs. In contrast, HIV-containing platelets fail to directly infect CD4+ T, unless infection is forced by the fusion inducer polybrene. Thus, in contrast to macrophages, CD4+ T cells are not targeted by HIV enclosed in platelets.
However, HIV-containing platelets might immunomodulate CD4+ T cell functions thereby triggering the immunological failure observed in cART-suppressed patients. Hence, platelet-T-cell conjugates form in the blood of HIV patients, suggesting that HIV-containing platelets could downregulate T-cell functions. Platelets are known to express adhesive proteins that not only promote platelet aggregation responsible for primary hemostasis, but also to mediate interactions with leukocytes, driving either inhibition of proliferation and differentiation of CD4+ T-cells into TH17, crucial in mediating chronic inflammation. Platelets can also shed microvesicles (ectosomes) which directly contact these lymphocytes, driving TH17 polarization of CD4+ T-cells and in turn an unbalanced TReg/TH17 ratio characteristic of InRs. Such TReg/TH17 unbalance might reflect a persistent inflammatory state that could translate in a cytotoxic/antiproliferative effect on CD4+ T-cells and ultimately immunological failure.
Very recently, we found that the number of platelets-CD4+ T-cells conjugates circulating in the blood of cART-treated HIV-infected patients is increased in InRs (virally suppressed and \<350 CD4+T-cells/μl) compared with immunological responders (IR, \>500 CD4+T-cells/μl). In addition, conjugates form more with TH17 in InR compared with IR, whereas conjugates form equally with TReg in the two InR and IR patients groups. These results indicate that InRs not only present a strong probability to have HIV-containing platelets but are also prone to form platelets-TH17 cells conjugates, suggesting a causal connection between association of HIV with platelets and platelet-driven immunomodulation of CD4+T-cells toward a TH17 profile. Whether these platelet-TH17 conjugates we observed form with full platelets or platelet ectosome (that both harbor CD41 used as platelet marker in our conjugate analyses) remains unknown.
Importantly, HIV RNA is only detected in circulating CD4+ T-cell reservoirs when latent proviral DNA is reactivated, suggesting that platelet-containing HIV does not conjugate with CD4+T cell in InR patients but rather with bystander platelets or platelet ectosomes (lacking HIV). Thus, immunomodulation of CD4+T cells in InRs might result from the interaction with these bystander platelet/ectosomes or ectosomes shed from HIV-containing platelets.
Platelets have been shown to exchange mRNA upon interaction with immune cells and tumors . Furthermore, transfer of functional mRNA and microRNA is so far demonstrated to be mediated by platelet ectosomes, targeting macrophage/monocytic and epithelial cells. Thus, transfer of messenger RNAs or microRNAs from platelets/ectosomes to macrophages and/or CD4+ T-cells could be the mechanism of platelet-dependent immunomodulation of target leukocytes. Platelets display a repertoire of mainly pro-inflammatory microRNAs such as miRNA-155 and miRNA-326, involved in NF-κB-mediated inflammatory macrophage responses 25 and TH17 cell-polarization. These miRNAs could be differentially expressed in platelets containing HIV and their eventual transfer to target immune cells could participate in immune cell dysfunction as observed in InRs. Furthermore, αIIb/ β3 mRNA are platelet-specific transcripts conserved in circulating platelets throughout their life-span, and can be exploited to tag leukocytes targeted by mRNA/microRNA of HIV-containing platelets.
Platelets are cleared by tissue macrophages in vivo in physiological or inflammatory contexts, what could represent a route for HIV to establish reservoirs in macrophages. We have shown that HIV sheltered in platelets can transfer infection to macrophages, in a process blocked by anti-αIIb/ β3 antibody Abciximab. This infection is productive as in turn, infection spreads replication-competent virus to non-infected CD4+ T-cells. This viral spread may increase the blood T-cell HIV reservoir, a hallmark of immunological failure as observed in InRs. In contrast, HIV-containing platelets fail to directly infect CD4+ T, unless infection is forced by the fusion inducer polybrene. Thus, in contrast to macrophages, CD4+ T cells are not targeted by HIV enclosed in platelets.
However, HIV-containing platelets might immunomodulate CD4+ T cell functions thereby triggering the immunological failure observed in cART-suppressed patients. Hence, platelet-T-cell conjugates form in the blood of HIV patients, suggesting that HIV-containing platelets could downregulate T-cell functions. Platelets are known to express adhesive proteins that not only promote platelet aggregation responsible for primary hemostasis, but also to mediate interactions with leukocytes, driving either inhibition of proliferation and differentiation of CD4+ T-cells into TH17, crucial in mediating chronic inflammation. Platelets can also shed microvesicles (ectosomes) which directly contact these lymphocytes, driving TH17 polarization of CD4+ T-cells and in turn an unbalanced TReg/TH17 ratio characteristic of InRs. Such TReg/TH17 unbalance might reflect a persistent inflammatory state that could translate in a cytotoxic/antiproliferative effect on CD4+ T-cells and ultimately immunological failure.
Very recently, we found that the number of platelets-CD4+ T-cells conjugates circulating in the blood of cART-treated HIV-infected patients is increased in InRs (virally suppressed and \<350 CD4+T-cells/μl) compared with immunological responders (IR, \>500 CD4+T-cells/μl). In addition, conjugates form more with TH17 in InR compared with IR, whereas conjugates form equally with TReg in the two InR and IR patients groups. These results indicate that InRs not only present a strong probability to have HIV-containing platelets but are also prone to form platelets-TH17 cells conjugates, suggesting a causal connection between association of HIV with platelets and platelet-driven immunomodulation of CD4+T-cells toward a TH17 profile. Whether these platelet-TH17 conjugates we observed form with full platelets or platelet ectosome (that both harbor CD41 used as platelet marker in our conjugate analyses) remains unknown.
Importantly, HIV RNA is only detected in circulating CD4+ T-cell reservoirs when latent proviral DNA is reactivated, suggesting that platelet-containing HIV does not conjugate with CD4+T cell in InR patients but rather with bystander platelets or platelet ectosomes (lacking HIV). Thus, immunomodulation of CD4+T cells in InRs might result from the interaction with these bystander platelet/ectosomes or ectosomes shed from HIV-containing platelets.
Platelets have been shown to exchange mRNA upon interaction with immune cells and tumors . Furthermore, transfer of functional mRNA and microRNA is so far demonstrated to be mediated by platelet ectosomes, targeting macrophage/monocytic and epithelial cells. Thus, transfer of messenger RNAs or microRNAs from platelets/ectosomes to macrophages and/or CD4+ T-cells could be the mechanism of platelet-dependent immunomodulation of target leukocytes. Platelets display a repertoire of mainly pro-inflammatory microRNAs such as miRNA-155 and miRNA-326, involved in NF-κB-mediated inflammatory macrophage responses 25 and TH17 cell-polarization. These miRNAs could be differentially expressed in platelets containing HIV and their eventual transfer to target immune cells could participate in immune cell dysfunction as observed in InRs. Furthermore, αIIb/ β3 mRNA are platelet-specific transcripts conserved in circulating platelets throughout their life-span, and can be exploited to tag leukocytes targeted by mRNA/microRNA of HIV-containing platelets.
Conditions
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HIV Seropositivity
Study Design
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Observational Model Type
COHORT
Study Time Perspective
PROSPECTIVE
Study Groups
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VIH positive patients without lymphoma
200 VIH positive patients without lymphoma
No interventions assigned to this group
VIH positive patients with lymphoma
20 VIH positive patients with lymphoma
No interventions assigned to this group
healthy volunteers
20 healthy volunteers
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
For all patients:
* aged ⩾ 18 years;
* patients who can read and understand information document.
For VIH positive patients without lymphoma:
* VIH positive patients with negative or positive viral load under cART since 1 year;
* patient under cART.
For VIH positive patients with lymphoma:
* VIH positive patient with negative viral load under cART since 1 year;
* patient with lymphoma.
For Healthy Volunteers:
* VIH negative patient (control) already included in clinical trial;
* patient major without haematological pathology.
* aged ⩾ 18 years;
* patients who can read and understand information document.
For VIH positive patients without lymphoma:
* VIH positive patients with negative or positive viral load under cART since 1 year;
* patient under cART.
For VIH positive patients with lymphoma:
* VIH positive patient with negative viral load under cART since 1 year;
* patient with lymphoma.
For Healthy Volunteers:
* VIH negative patient (control) already included in clinical trial;
* patient major without haematological pathology.
Exclusion Criteria
* patient \< 18 years;
* Unable to read and understand information document.
* Unable to read and understand information document.
Minimum Eligible Age
18 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
Yes
Sponsors
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Institut National de la Santé Et de la Recherche Médicale, France
OTHER_GOV
Sponsor Role
collaborator
Assistance Publique - Hôpitaux de Paris
OTHER
Sponsor Role
lead
Responsible Party
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Responsibility Role
SPONSOR
Principal Investigators
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Claude Capron, MD
Role: PRINCIPAL_INVESTIGATOR
Service Hématologie Immunologie, Hôpital Ambroise Paré
MORGANE BOMSEL, MD
Role: STUDY_DIRECTOR
Unité CNRS UMR 8104, INSERM U1016, Laboratoire Entrée muqueuse du VIH et Immunité muqueuse, Département Infection, Immunité et Inflammation, Institut Cochin Université Paris Descartes
Locations
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Service Hématologie Immunologie, Hôpital Ambroise Paré
Boulogne-Billancourt, , France
Site Status
RECRUITING
Countries
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France
Central Contacts
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References
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Mann M, Mehta A, Zhao JL, Lee K, Marinov GK, Garcia-Flores Y, Lu LF, Rudensky AY, Baltimore D. An NF-kappaB-microRNA regulatory network tunes macrophage inflammatory responses. Nat Commun. 2017 Oct 11;8(1):851. doi: 10.1038/s41467-017-00972-z.
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Rowley JW, Chappaz S, Corduan A, Chong MM, Campbell R, Khoury A, Manne BK, Wurtzel JG, Michael JV, Goldfinger LE, Mumaw MM, Nieman MT, Kile BT, Provost P, Weyrich AS. Dicer1-mediated miRNA processing shapes the mRNA profile and function of murine platelets. Blood. 2016 Apr 7;127(14):1743-51. doi: 10.1182/blood-2015-07-661371. Epub 2016 Jan 14.
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Du C, Liu C, Kang J, Zhao G, Ye Z, Huang S, Li Z, Wu Z, Pei G. MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis. Nat Immunol. 2009 Dec;10(12):1252-9. doi: 10.1038/ni.1798. Epub 2009 Oct 18.
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Zhu A, Real F, Zhu J, Greffe S, de Truchis P, Rouveix E, Bomsel M, Capron C. HIV-Sheltering Platelets From Immunological Non-Responders Induce a Dysfunctional Glycolytic CD4+ T-Cell Profile. Front Immunol. 2022 Feb 11;12:781923. doi: 10.3389/fimmu.2021.781923. eCollection 2021.
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BACKGROUND
Real F, Capron C, Sennepin A, Arrigucci R, Zhu A, Sannier G, Zheng J, Xu L, Masse JM, Greffe S, Cazabat M, Donoso M, Delobel P, Izopet J, Eugenin E, Gennaro ML, Rouveix E, Cramer Borde E, Bomsel M. Platelets from HIV-infected individuals on antiretroviral drug therapy with poor CD4+ T cell recovery can harbor replication-competent HIV despite viral suppression. Sci Transl Med. 2020 Mar 18;12(535):eaat6263. doi: 10.1126/scitranslmed.aat6263.
Reference Type
BACKGROUND
Other Identifiers
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19CCN-VIH-Plaquettes
Identifier Type: -
Identifier Source: org_study_id
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