Cell Biology of HIV: From Immune Cells Dysregulation to HIV-Related Cardiovascular Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 5700

Special Issue Editor


E-Mail Website1 Website2
Guest Editor
INSERM1096, Rouen, France
Interests: cardio-immunology; immune checkpoint inhibitor immune related adverse events (ICI-irAEs); autoimmunity; cardiac lymphatic; Lymphoid Germinal Center (Tfh)

Special Issue Information

Dear Colleagues,

Human immunodeficiency virus (HIV) remains a worldwide burden despite available treatments, such as antiretroviral therapy (ART). ART can durably suppress HIV replication; however, it is not curative as integrated HIV genome persists within CD4+ T cells and perhaps other immune cells. The virus induces dysregulations in major immune cells (T follicular helper (Tfh), CD8+ T cells, macrophages, dendritic cells (DC) from myeloid to plasmacytoid (pDC)) and uses cell-to-cell contact for transmission and dissemination. Thus, HIV infection is accompanied by persistent immune activation despite effective ART and maintained viral suppression. This constant activation of both the innate and adaptive immune systems results in low grade inflammation, leading to circulating proinflammatory and profibrotic cytokines, which may contribute to cardiac and endothelial dysfunction, hypercoagulation, and fibrotic remodeling and increase the risk of cardiovascular disease (CVD) onset in people living with HIV. In fact, HIV+ patients with access to modern ART face a two-fold increased risk of heart failure as compared to non-HIV-infected individuals.

This Special Issue will examine how HIV interferes with immune cell subsets (Tfh, CD8+ T Cells, B cells and myeloid cells) activity in vitro and in vivo after traditional ART or early onset of ART during acute HIV infection. Finally, the special issue will emphasize how HIV interferes with cardiomyocytes function in vitro and how HIV-impaired immune cells activity may lead to higher risk of CVD. 

Dr. Virginie Tardif
Guest Editor

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Keywords

  • HIV-dysregulated immunity (Tfh, DC, B cells, myeloid cells)
  • cell infection
  • transmission
  • acute HIV
  • chronic HIV
  • HIV-related CVD
  • HIV-cardiotoxicity

Published Papers (2 papers)

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Research

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26 pages, 6613 KiB  
Article
HIV-1 Infection of Long-Lived Hematopoietic Precursors In Vitro and In Vivo
by Sebastian Renelt, Patrizia Schult-Dietrich, Hanna-Mari Baldauf, Stefan Stein, Gerrit Kann, Markus Bickel, Ulrikke Kielland-Kaisen, Halvard Bonig, Rolf Marschalek, Michael A. Rieger, Ursula Dietrich and Ralf Duerr
Cells 2022, 11(19), 2968; https://doi.org/10.3390/cells11192968 - 23 Sep 2022
Cited by 10 | Viewed by 2694
Abstract
Latent reservoirs in human-immunodeficiency-virus-1 (HIV-1)-infected individuals represent a major obstacle in finding a cure for HIV-1. Hematopoietic stem and progenitor cells (HSPCs) have been described as potential HIV-1 targets, but their roles as HIV-1 reservoirs remain controversial. Here we provide additional evidence for [...] Read more.
Latent reservoirs in human-immunodeficiency-virus-1 (HIV-1)-infected individuals represent a major obstacle in finding a cure for HIV-1. Hematopoietic stem and progenitor cells (HSPCs) have been described as potential HIV-1 targets, but their roles as HIV-1 reservoirs remain controversial. Here we provide additional evidence for the susceptibility of several distinct HSPC subpopulations to HIV-1 infection in vitro and in vivo. In vitro infection experiments of HSPCs were performed with different HIV-1 Env-pseudotyped lentiviral particles and with replication-competent HIV-1. Low-level infection/transduction of HSPCs, including hematopoietic stem cells (HSCs) and multipotent progenitors (MPP), was observed, preferentially via CXCR4, but also via CCR5-mediated entry. Multi-lineage colony formation in methylcellulose assays and repetitive replating of transduced cells provided functional proof of susceptibility of primitive HSPCs to HIV-1 infection. Further, the access to bone marrow samples from HIV-positive individuals facilitated the detection of HIV-1 gag cDNA copies in CD34+ cells from eight (out of eleven) individuals, with at least six of them infected with CCR5-tropic HIV-1 strains. In summary, our data confirm that primitive HSPC subpopulations are susceptible to CXCR4- and CCR5-mediated HIV-1 infection in vitro and in vivo, which qualifies these cells to contribute to the HIV-1 reservoir in patients. Full article
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Review

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15 pages, 1438 KiB  
Review
HIV-Related Myocardial Fibrosis: Inflammatory Hypothesis and Crucial Role of Immune Cells Dysregulation
by Eman Teer, Leanne Dominick, Nyasha C. Mukonowenzou and M. Faadiel Essop
Cells 2022, 11(18), 2825; https://doi.org/10.3390/cells11182825 - 9 Sep 2022
Cited by 6 | Viewed by 2314
Abstract
Although the underlying mechanisms driving human immunodeficiency virus (HIV)-mediated cardiovascular diseases (CVD) onset and progression remain unclear, the role of chronic immune activation as a significant mediator is increasingly being highlighted. Chronic inflammation is a characteristic feature of CVD and considered a contributor [...] Read more.
Although the underlying mechanisms driving human immunodeficiency virus (HIV)-mediated cardiovascular diseases (CVD) onset and progression remain unclear, the role of chronic immune activation as a significant mediator is increasingly being highlighted. Chronic inflammation is a characteristic feature of CVD and considered a contributor to diastolic dysfunction, heart failure, and sudden cardiac death. This can trigger downstream effects that result in the increased release of pro-coagulant, pro-fibrotic, and pro-inflammatory cytokines. Subsequently, this can lead to an enhanced thrombotic state (by platelet activation), endothelial dysfunction, and myocardial fibrosis. Of note, recent studies have revealed that myocardial fibrosis is emerging as a mediator of HIV-related CVD. Together, such factors can eventually result in systolic and diastolic dysfunction, and an increased risk for CVD. In light of this, the current review article will focus on (a) the contributions of a chronic inflammatory state and persistent immune activation, and (b) the role of immune cells (mainly platelets) and cardiac fibrosis in terms of HIV-related CVD onset/progression. It is our opinion that such a focus may lead to the development of promising therapeutic targets for the treatment and management of CVD in HIV-positive patients. Full article
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