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Viruses
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HIV Neurological Disorders: 2nd Edition
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HIV Neurological Disorders: 2nd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 7364

Special Issue Editor

Dr. Frank Denaro

E-Mail Website
Guest Editor
Department of Biology, Morgan State University, Baltimore, MD 21251, USA
Interests: neuroscience; neuropathology; cell biology; HIV
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It became apparent from the first Special Issue on HIV neurological disorders (https://www.mdpi.com/journal/viruses/special_issues/HIV_Neurological_Disorders) that there are many unresolved neurologic and psychological challenges associated with HIV that are worthy of discussion. These challenges include, but are not limited to, clinical manifestations, quantitative diagnostic measures, pathological mechanisms and treatment developments. This second Special Issue on HIV Neurological Disorders can address the different challenges clinicians and researchers in the field are now facing.

The mechanisms for the production of HIV-related neurologic disorders remain elusive and complex. In many parts of the world, opportunistic infections still present a continued challenge. Where treatment is available, patients may eventually present with HIV noninfectious comorbidities. Both these situations need to be addressed, but an underlying point in both is the presence of HIV-associated inflammation. In addition, abuse of drugs can complicate treatment and lead to poor outcomes, particularly where the nervous system is concerned. 

Chronic inflammation associated with HIV infection is the main candidate in regard to HIV neurological comorbidities, but there is a need for both clinical and basic science research addressing all aspects of HIV neurologic disorders.

Dr. Frank Denaro
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 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. Viruses is an international peer-reviewed open access monthly 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 2600 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

  • neuroinflammation
  • chronic HIV inflammation
  • HIV reservoir
  • HIV proteins
  • HIV receptors
  • HIV models
  • drugs of abuse
  • AIDS dementia complex
  • HIV noninfectious comorbidities
  • HIV healthcare disparities
  • HIV neuropathology

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Related Special Issue

Published Papers (3 papers)

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Research

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14 pages, 819 KB  
Article
Neurocognitive Impairment in ART-Experienced People Living with HIV: An Analysis of Clinical Risk Factors, Injection Drug Use, and the sCD163
by Syed Zaryab Ahmed, Faiq Amin, Nida Farooqui, Zhannur Omarova, Syed Faisal Mahmood, Qurat ul ain Khan, Haider A. Naqvi, Aida Mumtaz, Saeeda Baig, Muhammad Rehan Khan, Sharaf A. Shah, Ali Hassan, Srinivasa Bolla, Shamim Mushtaq and Syed Hani Abidi
Viruses 2025, 17(9), 1232; https://doi.org/10.3390/v17091232 - 10 Sep 2025
Viewed by 712
Abstract
Background: In people living with HIV (PLHIV), ongoing neuronal injury has shown a correlation with elevated levels of soluble markers of immune activation, such as sCD163. Additionally, various risk factors, such as injection drug use (IDU), can independently affect immune and cognitive functions, [...] Read more.
Background: In people living with HIV (PLHIV), ongoing neuronal injury has shown a correlation with elevated levels of soluble markers of immune activation, such as sCD163. Additionally, various risk factors, such as injection drug use (IDU), can independently affect immune and cognitive functions, leading to neurocognitive impairment (NCI). However, the potential sCD163-IDU-NCI axis in ART-experienced PLHIV is not clear. This study aims to determine NCI prevalence and investigate the interplay between risk factors and sCD163 in Pakistani PLHIV. Methods: For this cross-sectional study, 150 PLHIV and 30 HIV-negative people who inject drugs (PWID) were recruited using a convenience sampling strategy. NCI screening was performed using the International HIV Dementia Scale (IHDS) tool. Blood samples from PLHIV were used to perform HIV recency testing using the Asante Rapid Recency Assay, and to evaluate sCD163 levels using ELISA. Sociodemographic and clinical data were collected from medical records. Subsequently, descriptive statistics were used to summarize data variables, while comparisons (two and multiple groups) between participants with and without NCI were conducted, respectively, using the Mann–Whitney test or Kruskal–Wallis test for continuous variables, and Fisher’s exact test for categorial variables. Receiver Operating Characteristic (ROC) curve analysis was performed to assess the discriminative ability of sCD163. Logistic regression was used to identify predictors of neurocognitive impairment. Results: The majority of PLHIV had IDU as a high-risk behavior. In PLHIV, the median age was 34.5 years (IQR: 30–41), ART duration was 35 months (IQR: 17–54), and median CD4 count was 326.5 cells/µL (IQR: 116–545.5). Long-term infections (>6 months post-seroconversion; median ART duration: 35 months; median CD4 counts: 326.5 cells/μL) were noted in 83.3% of PLHIV. IHDS-based screening showed that 83.33% (all PLHIV) and 50% (PLHIV with no IDU history) scored ≤ 9 on the IHDS, suggestive of NCI. IHDS-component analysis showed the memory recall to be significantly affected in PLHIV compared to controls (median score 3.2 versus 3.7, respectively, p < 0.001). Regression analysis showed only long-term infection (OR: 2.99, p = 0.03) to be significantly associated with neurocognitive impairment. sCD163 levels were significantly lower in PLHIV with NCI (mean = 7.48 ng/mL, SD = 7.05) compared to those without NCI (mean = 14.82 ng/mL, SD = 8.23; p < 0.0001), with an AUC of 0.803 (95% CI: 0.72–0.88). However, after adjusting for IDU history, the regression analysis showed an odds ratio for sCD163 of 0.998 (95% CI: 0.934, 1.067, p = 0.957), indicating no association between sCD163 levels and NCI. Conclusion: This study reports a high prevalence of NCI in Pakistani PLHIV, and no association between sCD163 and neurocognitive impairment in PLHIV after adjustment for a history of IDU. Long-term infection and IDU were significantly linked to NCI, while only IDU was associated with lower sCD163 levels, regardless of NCI. Full article
(This article belongs to the Special Issue HIV Neurological Disorders: 2nd Edition)
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17 pages, 1553 KB  
Article
Microglia Exhibit a Unique Intact HIV Reservoir in Human Postmortem Brain Tissue
by Marieke M. Nühn, Stephanie B. H. Gumbs, Pauline J. Schipper, Irene Drosou, Lavina Gharu, Ninée V. E. J. Buchholtz, Gijsje J. L. J. Snijders, Frederieke A. J. Gigase, Annemarie M. J. Wensing, Jori Symons, Lot D. de Witte and Monique Nijhuis
Viruses 2025, 17(4), 467; https://doi.org/10.3390/v17040467 - 25 Mar 2025
Cited by 1 | Viewed by 1531
Abstract
A proviral reservoir persists within the central nervous system (CNS) of people with HIV, but its characteristics remain poorly understood. Research has primarily focused on cerebrospinal fluid (CSF), as acquiring brain tissue is challenging. We examined size, cellular tropism, and infection-dynamics of the [...] Read more.
A proviral reservoir persists within the central nervous system (CNS) of people with HIV, but its characteristics remain poorly understood. Research has primarily focused on cerebrospinal fluid (CSF), as acquiring brain tissue is challenging. We examined size, cellular tropism, and infection-dynamics of the viral reservoir in post-mortem brain tissue from five individuals on and off antiretroviral therapy (ART) across three brain regions. Microglia-enriched fractions (CD11b+) were isolated and levels of intact proviral DNA were quantified (IPDA). Full-length envelope reporter viruses were generated and characterized in CD4+ T cells and monocyte-derived microglia. HIV DNA was observed in microglia-enriched fractions of all individuals, but intact proviruses were identified only in one ART-treated individual, representing 15% of the total proviruses. Phenotypic analyses of clones from this individual showed that 80% replicated efficiently in microglia and CD4+ T cells, while the remaining viruses replicated only in CD4+ T cells. No region-specific effects were observed. These results indicate a distinct HIV brain reservoir in microglia for all individuals, although intact proviruses were detected in only one. Given the unique immune environment of the CNS, the characteristics of microglia, and the challenges associated with targeting these cells, the CNS reservoir should be considered in cure strategies. Full article
(This article belongs to the Special Issue HIV Neurological Disorders: 2nd Edition)
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Review

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26 pages, 1668 KB  
Review
Neuroinflammation, Blood–Brain Barrier, and HIV Reservoirs in the CNS: An In-Depth Exploration of Latency Mechanisms and Emerging Therapeutic Strategies
by Noor Said and Vishwanath Venketaraman
Viruses 2025, 17(4), 572; https://doi.org/10.3390/v17040572 - 16 Apr 2025
Cited by 1 | Viewed by 3920
Abstract
Despite the success of antiretroviral therapy (ART) in suppressing viral replication in the blood, HIV persists in the central nervous system (CNS) and causes chronic neurocognitive impairment, a hallmark of HIV-associated neurocognitive disorders (HAND). This review looks at the complex interactions among HIV, [...] Read more.
Despite the success of antiretroviral therapy (ART) in suppressing viral replication in the blood, HIV persists in the central nervous system (CNS) and causes chronic neurocognitive impairment, a hallmark of HIV-associated neurocognitive disorders (HAND). This review looks at the complex interactions among HIV, the blood–brain barrier (BBB), neuroinflammation, and the roles of viral proteins, immune cell trafficking, and pro-inflammatory mediators in establishing and maintaining latent viral reservoirs in the CNS, particularly microglia and astrocytes. Key findings show disruption of the BBB, monocyte infiltration, and activation of CNS-resident cells by HIV proteins like Tat and gp120, contributing to the neuroinflammatory environment and neuronal damage. Advances in epigenetic regulation of latency have identified targets like histone modifications and DNA methylation, and new therapeutic strategies like latency-reversing agents (LRAs), gene editing (CRISPR/Cas9), and nanoparticle-based drug delivery also offer hope. While we have made significant progress in understanding the molecular basis of HIV persistence in the CNS, overcoming the challenges of BBB penetration and neuroinflammation is key to developing effective therapies. Further research into combination therapies and novel drug delivery systems will help improve outcomes for HAND patients and bring us closer to a functional cure for HIV. Full article
(This article belongs to the Special Issue HIV Neurological Disorders: 2nd Edition)
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