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Cellular and Molecular Mechanisms of HIV-1-Associated Cardiovascular Disease
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Cellular and Molecular Mechanisms of HIV-1-Associated Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 4881

Special Issue Editors

Prof. Dr. Xuebin Qin

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, School of Medicine, Tulane University, New Orleans, LA 70112, USA
Interests: HIV-1 therapy; Innate immunity; HIV-associated cardiovascular diseases
Dr. Namita Rout

E-Mail Website
Guest Editor
Division of Microbiology, Tulane National Primate Research Center, Tulane University, Covington, LA 70433, USA
Interests: HIV pathogenesis and cure; HIV/TB coinfection; aging mucosal immunity and inflammation of aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the era of combination antiretroviral therapy (cART), individuals living with HIV (PLWH) face a twofold higher likelihood of developing cardiovascular disease (CVD) compared to those without HIV. The global prevalence of CVD linked to HIV has tripled over the last two decades. While HIV-related CVD used to primarily manifest as conditions such as dilated cardiomyopathy, pericardial disease, and pulmonary hypertension, the widespread use of cART has shifted the pattern towards atherosclerosis-related issues, including heart attack, stroke, and heart failure. This increased CVD risk in PLWH is attributed to chronic HIV-driven inflammation. Although clinical research is growing, experimental studies on this subject are scarce.

An improved understanding of the mechanisms driving the development of CVD in PLWH could lead to better strategies for its prevention. For instance, this might involve targeting specific molecules within pathways that worsen the disease and developing new immunomodulatory therapies. The main goal of this Special Issue is to present a comprehensive overview of the current understanding of the origins of CVD linked to HIV-1. As a result, we encourage the submission of original research and review papers that focus on a range of subjects, including, though not confined to, the following topics:

  1. Identification of novel biomarkers of HIV-1-associated CVD;
  2. Changes in immune cell functions and signaling pathways associated with CVD in HIV or SIV infection;
  3. Experimental model studies of HIV-associated CVD;
  4. Effects of cART, diet, microbiota, etc., on atherosclerosis during HIV/SIV infection;
  5. Clinical studies on cardiovascular disease and HIV.

Since IJMS is a journal of molecular science, pure clinical studies will not be suitable for our journal. But, clinical submissions which feature biomolecular experiments are welcomed.

Prof. Dr. Xuebin Qin
Dr. Namita Rout
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • HIV
  • SIV
  • nonhuman primates
  • atherosclerosis
  • myocardial infarction (MI)
  • stroke
  • heart failure
  • immune activation
  • macrophage/monocyte activation
  • molecular and cellular mechanisms
  • chronic infection
  • animal models
  • clinical studies

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Published Papers (3 papers)

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Research

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21 pages, 5700 KiB  
Article
Diastolic Dysfunction with Vascular Deficits in HIV-1-Infected Female Humanized Mice Treated with Antiretroviral Drugs
by Fadhel A. Alomar, Prasanta K. Dash, Mahendran Ramasamy, Zachary L. Venn, Sean R. Bidasee, Chen Zhang, Bryan T. Hackfort, Santhi Gorantla and Keshore R. Bidasee
Int. J. Mol. Sci. 2025, 26(8), 3801; https://doi.org/10.3390/ijms26083801 - 17 Apr 2025
Viewed by 185
Abstract
Early-onset heart failure is a major treat to healthy aging individuals with HIV-1 infection. Women with HIV-1 infection (WLWH) are especially vulnerable and develop heart failure with preserved ejection fraction (HFpEF), of which left ventricular diastolic dysfunction, vascular deficits, myocardial infarction, and fibrosis [...] Read more.
Early-onset heart failure is a major treat to healthy aging individuals with HIV-1 infection. Women with HIV-1 infection (WLWH) are especially vulnerable and develop heart failure with preserved ejection fraction (HFpEF), of which left ventricular diastolic dysfunction, vascular deficits, myocardial infarction, and fibrosis are major components. HIV-infected rodent models that exhibit these pathophysiological features remain under-reported, and this has left a void in our understanding of their molecular causes and therapeutic strategies to blunt its development. Here, we show that female NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ humanized mice (Hu-mice) infected with HIV-1ADA and treated for 13 weeks with dolutegravir (DTG)/tenofovir disoproxil fumarate (TDF)/emtricitabine (FTC) develop progressive diastolic dysfunction with preserved ejection fraction (E:A ratio, E:e′, IVRT, left atrial volume and global longitudinal strain increased by 32.1 ± 5.1%, 28.2 ± 5.6%, 100.2 ± 12.6%, 26.6 ± 4.2% and 32.5 ± 4.3%, respectively). In vivo photoacoustic imaging revealed a 30.4 ± 6.8% reduction in saturated oxygenated hemoglobin in the anterior wall of the heart. The ex vivo analysis of hearts showed a reduction in density of perfused microvessels/ischemia (30.6 ± 6.2%) with fibrosis (20.2 ± 1.2%). The HIF-1α level was increased 2.6 ± 0.5-fold, while inflammation-induced serum semicarbazide amine oxidase and glycolysis byproduct methylglyoxal increased 2-fold and 2.1-fold, respectively. Treating H9C2 cardiac myocytes with DTG, FTC and TDF dose-dependently increased expression of HIF-1α. These data show that HIV-infected Hu-mice treated with DTG/TDF/FTC for thirteen weeks develop cardiac diastolic dysfunction, with vascular deficits, ischemia, and fibrosis like those reported in women living with HIV-1 infection (WLWH). They also show that DTG, TDF, and FTC treatment can increase total HIF-1α in H9C2 cells. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of HIV-1-Associated Cardiovascular Disease)
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14 pages, 1897 KiB  
Article
The Association between IL-1β and IL-18 Levels, Gut Barrier Disruption, and Monocyte Activation during Chronic Simian Immunodeficiency Virus Infection and Long-Term Suppressive Antiretroviral Therapy
by Siva Thirugnanam, Chenxiao Wang, Chen Zheng, Brooke F. Grasperge, Prasun K. Datta, Jay Rappaport, Xuebin Qin and Namita Rout
Int. J. Mol. Sci. 2024, 25(16), 8702; https://doi.org/10.3390/ijms25168702 - 9 Aug 2024
Viewed by 1651
Abstract
HIV-induced persistent immune activation is a key mediator of inflammatory comorbidities such as cardiovascular disease (CVD) and neurocognitive disorders. While a preponderance of data indicate that gut barrier disruption and microbial translocation are drivers of chronic immune activation, the molecular mechanisms of this [...] Read more.
HIV-induced persistent immune activation is a key mediator of inflammatory comorbidities such as cardiovascular disease (CVD) and neurocognitive disorders. While a preponderance of data indicate that gut barrier disruption and microbial translocation are drivers of chronic immune activation, the molecular mechanisms of this persistent inflammatory state remain poorly understood. Here, utilizing the nonhuman primate model of Human Immunodeficiency Virus (HIV) infection with suppressive antiretroviral therapy (ART), we investigated activation of inflammasome pathways and their association with intestinal epithelial barrier disruption (IEBD). Longitudinal blood samples obtained from rhesus macaques with chronic SIV infection and long-term suppressive ART were evaluated for IEBD biomarkers, inflammasome activation (IL-1β and IL-18), inflammatory cytokines, and triglyceride (TG) levels. Activated monocyte subpopulations and glycolytic potential were investigated in peripheral blood mononuclear cells (PBMCs). During the chronic phase of treated SIV infection, elevated levels of plasma IL-1β and IL-18 were observed following the hallmark increase in IEBD biomarkers, intestinal fatty acid-binding protein (IFABP) and LPS-binding protein (LBP). Further, significant correlations of plasma IFABP levels with IL-1β and IL-18 were observed between 10 and 12 months of ART. Higher levels of sCD14, IL-6, and GM-CSF, among other inflammatory mediators, were also observed only during the long-term SIV + ART phase along with a trend of increase in the frequencies of activated CD14+CD16+ intermediate monocyte subpopulations. Lastly, we found elevated levels of blood TG and higher glycolytic capacity in PBMCs of chronic SIV-infected macaques with long-term ART. The increase in circulating IL-18 and IL-1β following IEBD and their significant positive correlation with IFABP suggest a connection between gut barrier disruption and inflammasome activation during chronic SIV infection, despite viral suppression with ART. Additionally, the increase in markers of monocyte activation, along with elevated TG and enhanced glycolytic pathway activity, indicates metabolic remodeling that could fuel metabolic syndrome. Further research is needed to understand the mechanisms by which gut dysfunction and inflammasome activation contribute to HIV-associated metabolic complications, enabling targeted interventions in people with HIV. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of HIV-1-Associated Cardiovascular Disease)
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Review

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31 pages, 4111 KiB  
Review
Inflammatory and Immune Mechanisms for Atherosclerotic Cardiovascular Disease in HIV
by Laura Hmiel, Suyu Zhang, Laventa M. Obare, Marcela Araujo de Oliveira Santana, Celestine N. Wanjalla, Boghuma K. Titanji, Corrilynn O. Hileman and Shashwatee Bagchi
Int. J. Mol. Sci. 2024, 25(13), 7266; https://doi.org/10.3390/ijms25137266 - 1 Jul 2024
Cited by 4 | Viewed by 2377
Abstract
Atherosclerotic vascular disease disproportionately affects persons living with HIV (PLWH) compared to those without. The reasons for the excess risk include dysregulated immune response and inflammation related to HIV infection itself, comorbid conditions, and co-infections. Here, we review an updated understanding of immune [...] Read more.
Atherosclerotic vascular disease disproportionately affects persons living with HIV (PLWH) compared to those without. The reasons for the excess risk include dysregulated immune response and inflammation related to HIV infection itself, comorbid conditions, and co-infections. Here, we review an updated understanding of immune and inflammatory pathways underlying atherosclerosis in PLWH, including effects of viral products, soluble mediators and chemokines, innate and adaptive immune cells, and important co-infections. We also present potential therapeutic targets which may reduce cardiovascular risk in PLWH. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of HIV-1-Associated Cardiovascular Disease)
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