Neuropathogenesis in HIV Infection: Mechanisms and Reservoirs

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 220

Special Issue Editor


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Guest Editor
Department of Molecular and Comparative Pathobiology and Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA
Interests: myeloid reservoirs in HIV; CNS immunology; chronic viral infections; immune mechanisms contributing to cognitive impairment

Special Issue Information

Dear Colleagues,

Substantial evidence suggests that HIV neuropathogenesis is primarily caused by chronic neuroinflammation, an inflammatory response in the brain that can lead to neuronal damage and degeneration, manifesting clinically as cognitive impairment in virally suppressed people with HIV (PWH).

HIV reservoirs in the central nervous system (CNS) are a central mechanism for chronic neuroinflammation. Defective and intact HIV genomes in brain macrophages contribute to neuropathogenesis by establishing a persistent viral source that drives neuroinflammation through viral RNA and protein production, contributing to blood–brain barrier (BBB) disruption, neuronal injury, cognitive decline, and potentially viral rebound, despite effective anti-retroviral therapy (ART). HIV enters the CNS via infected CD4+ T cells and monocytes within the first week of infection when the virus is detectable in both the cerebrospinal fluid (CSF) and brain. While ART suppresses HIV replication, ART penetration into the CNS is highly variable, and HIV RNA can be detected in CSF and brain tissue, contributing to ongoing neuroinflammation. This is likely further exacerbated by infected immune cells continuously crossing the BBB throughout ART and contributing to the maintenance of CNS reservoirs. However, HIV reservoirs are not the only mechanism contributing to the chronic neuroinflammation in PWH; additional contributions include HIV-associated comorbidities and aging.

The goal of this Special Issue will be to highlight our current understanding of the mechanisms associated with neuropathogenesis in HIV infection, with a central focus on HIV reservoirs and additional aspects that contribute to neuroinflammation. Topics of interest include, but are not limited to, the following:

  • Peripheral and CNS reservoirs and their role in neuroinflammation and clinical outcomes;
  • Mechanistic insights into HIV/SIV-associated neuroinflammation using in vitro assays and in vivo models;
  • In vivo studies on HIV-associated co-morbidities and aging and their associations with neuropathogenesis and neuroinflammation.

Dr. Rebecca T. Veenhuis
Guest Editor

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Keywords

  • HIV-associated neuroinflammation
  • HIV reservoirs
  • HIV-associated neuropathogenesis
  • HIV-associated comorbidities

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This special issue is now open for submission.
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