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Cells
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Immune Response in HIV Infection, Pathogenesis and Persistence
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Immune Response in HIV Infection, Pathogenesis and Persistence

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

Deadline for manuscript submissions: 20 March 2026 | Viewed by 2190

Special Issue Editor

Dr. Suvadip Mallick

E-Mail Website
Guest Editor
Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Interests: immunology; T cell biology; host–pathogen interaction; viral immunology; parasite immunology; virus pathogenesis and persistence

Special Issue Information

Dear Colleagues,

HIV infection exerts a profound impact on the immune system, triggering chronic inflammation and persistent immune activation that endure even with antiretroviral therapy (ART). This Special Issue, "Immune Response in HIV Infection, Pathogenesis and Persistence", delves into the intricate interplay between HIV and the immune system, with a focus on the molecular and cellular mechanisms driving immune responses and their implications for disease progression and therapeutic interventions. We welcome submissions that explore the role of immune checkpoints, the effects of chronic inflammation on immune cell functionality, and innovative therapeutic approaches aimed at enhancing immune reconstitution and mitigating immune activation. By bringing together cutting-edge research, this issue aims to provide a comprehensive overview of the field, showcasing recent breakthroughs and charting future directions for advancing our understanding and treatment of HIV-related immune dysregulation.

Dr. Suvadip Mallick
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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 infection
  • immune response
  • chronic inflammation
  • immune activation
  • antiretroviral therapy (ART)
  • immune reconstitution
  • immune checkpoints

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Published Papers (2 papers)

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Research

21 pages, 6176 KB  
Article
Description of T-Cell and Monocyte Populations in the Circulation of People with HIV Prior to AIDS-NHL Diagnosis
by Laura E. Martínez, Begoña Comin-Anduix, Miriam Güemes-Aragon, Javier Ibarrondo, Roger Detels, Matthew J. Mimiaga and Marta Epeldegui
Cells 2025, 14(20), 1608; https://doi.org/10.3390/cells14201608 - 16 Oct 2025
Viewed by 586
Abstract
People with HIV (PWH) are at an increased risk for AIDS-associated non-Hodgkin lymphoma (AIDS-NHL); however, the immune signatures underlying this risk are not well understood. In this study, we utilized mass cytometry by time-of-flight (CyTOF) to analyze T-cells and monocytes in the PBMCs [...] Read more.
People with HIV (PWH) are at an increased risk for AIDS-associated non-Hodgkin lymphoma (AIDS-NHL); however, the immune signatures underlying this risk are not well understood. In this study, we utilized mass cytometry by time-of-flight (CyTOF) to analyze T-cells and monocytes in the PBMCs of treatment-naïve PWH, including those 3 to 36 months before an AIDS-NHL diagnosis (HIV-positive pre-NHL), as well as people without HIV (PWoH). Mass cytometry is an advanced single-cell analysis platform that combines flow cytometry principles with mass spectrometry. Unlike conventional flow cytometry, this technology employs antibodies conjugated to unique metal isotopes instead of fluorescent markers, enabling simultaneous measurement of over 40 distinct cellular markers per individual cell without spectral overlap limitations. Participants were enrolled at the Los Angeles site of the MACS/WIHS Combined Cohort Study (MWCCS). Unsupervised clustering and Uniform Manifold Approximation and Projection (UMAP) analysis identified CD3+ T-cell and CD14+ monocyte metaclusters, and Spearman’s rank correlation assessed their relationships with B-cell subsets exhibiting aberrant phenotypes. We observed elevated levels of CD8+CD20+ T-cells, CD8+CD14+ T-cells, and M2-like CD14+CD163+ monocytes in HIV-positive pre-NHL individuals compared to HIV-negative controls. Positive correlations were found between CD19+ AICDA+ cMYC+ B-cells and M1-like CD14+cMYC+ monocytes (metacluster, MC02), and between metaclusters of CD8+PD-1+CD27+CXCR4− T-cells (MC05) and CD4+FoxP3+PD-1+CD27+CD28+CXCR4− ICOS+ T-cells (MC08). In addition, a different CD19+ B-cell metacluster (FoxP3+AICDA+cMYC+) was positively associated with a metacluster of CD8+PD-1+CD27+CD28+CXCR4+ T-cells (MC03). Moreover, the metacluster of CD8+PD-1+CD27+CXCR4− T-cells (MC05) negatively correlated with M2-like CD14+CD163+ monocytes (MC06), while CD8+CD14+ T-cells positively correlated with AICDA+ Bregs and IL-10+ B-regs in HIV-positive pre-NHL individuals. Unsupervised analysis revealed increased frequencies of CD8+CD20+ T-cells in HIV-positive individuals compared to HIV-negative controls. These immune alterations provide valuable insights into potential biomarkers for early detection, monitoring, and therapeutic strategies for AIDS-NHL. Full article
(This article belongs to the Special Issue Immune Response in HIV Infection, Pathogenesis and Persistence)
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20 pages, 2441 KB  
Article
Dysfunction and Metabolic Reprogramming of Gut Regulatory T Cells in HIV-Infected Immunological Non-Responders
by Minrui Yu, Mengmeng Qu, Zerui Wang, Cheng Zhen, Baopeng Yang, Yi Zhang, Huihuang Huang, Chao Zhang, Jinwen Song, Xing Fan, Ruonan Xu, Yan-Mei Jiao and Fu-Sheng Wang
Cells 2025, 14(15), 1164; https://doi.org/10.3390/cells14151164 - 29 Jul 2025
Cited by 2 | Viewed by 1216
Abstract
Disruption of the gut microenvironment is a hallmark of HIV infection, where regulatory T cells (Tregs) play a critical role in maintaining gut homeostasis. However, the mechanisms by which gut Tregs contribute to immune reconstitution failure in HIV-infected individuals remain poorly understood. In [...] Read more.
Disruption of the gut microenvironment is a hallmark of HIV infection, where regulatory T cells (Tregs) play a critical role in maintaining gut homeostasis. However, the mechanisms by which gut Tregs contribute to immune reconstitution failure in HIV-infected individuals remain poorly understood. In this study, we employed single-cell RNA sequencing (scRNA-seq) to analyze gut Treg populations across three cohorts: eight immunological responders (IRs), three immunological non-responders (INRs), and four HIV-negative controls (NCs). Our findings revealed that INRs exhibit an increased proportion of gut Tregs but with significant functional impairments, including reduced suppressive capacity and heightened apoptotic activity. Notably, these Tregs underwent metabolic reprogramming in INRs, marked by an upregulation of glycolysis-related genes and a downregulation of the oxidative phosphorylation (OXPHOS) pathway. Additionally, both the abundance of short-chain fatty acid (SCFA)-producing bacteria and SCFA concentrations were reduced in INRs. In vitro SCFA supplementation restored Treg function by enhancing suppressive capacity, reducing early apoptosis, and rebalancing cellular energy metabolism from glycolysis to OXPHOS. These findings provide a comprehensive characterization of gut Treg dysfunction in INRs and underscore the therapeutic potential of targeting gut Tregs through microbiota and metabolite supplementation to improve immune reconstitution in HIV-infected individuals. Full article
(This article belongs to the Special Issue Immune Response in HIV Infection, Pathogenesis and Persistence)
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