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The Interplay Between Immunity, Infection, and Neurocognitive Disorders

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 June 2025) | Viewed by 735

Special Issue Editor


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Guest Editor
Department of Neurology, Medical School, University of Cyprus, P.O. Box 20537, Nicosia 1678, Cyprus
Interests: infection; immunity; cognition; computational biology; neuroimmunology; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

A growing body of research has outlined the interplay between immunity, infection, and neurocognitive disorders. The COVID-19 pandemic provided significant impetus in advancing our understanding of this triple connection, with exposure to pathogens beyond SARS-CoV-2 having been consistently linked to an increased risk of neurodegenerative disease and cognitive impairment. Big data and translational studies have narrowed the gap between observation and mechanism for the connections between pathogen exposure and cognitive sequelae. In this Special Issue, we will attempt to decipher the multi-modal relationships and possible causative mechanisms by which host–pathogen interactions, and their specific footprints, impact the development of cognitive impairment. Authors of original studies, both clinical and translational, case reports, as well as high-quality reviews, are welcome to submit. Beyond long COVID, studies focusing on neurocognitive disorders arising from other pathogens will also be welcome.

Dr. George D. Vavougios
Guest Editor

Manuscript Submission Information

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Keywords

  • immunity
  • autoimmunity
  • cognition
  • cognitive impairment
  • infection
  • neurogeneration
  • neuroinflammation
  • computational biology
  • translational studies
  • meta-analysis

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Published Papers (1 paper)

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Research

18 pages, 1095 KB  
Article
In Vitro Model of the Human Blood–Brain Barrier to Explore HTLV-1 Immunopathogenesis
by Ana Beatriz Guimarães, Lucas Bernardo-Menezes, Elisa Azevedo, Almerinda Agrelli, Poliana Silva, Marília Sena, Waldecir Araújo Júnior, George Diniz, Wyndly Daniel Gaião, Claudio Rodrigues, Marton Cavalcante, Lúcio Roberto Castellano, Joelma Souza, Paula Magalhães, Antonio Carlos Vallinoto and Clarice Morais
Curr. Issues Mol. Biol. 2025, 47(10), 818; https://doi.org/10.3390/cimb47100818 - 3 Oct 2025
Viewed by 526
Abstract
Cellular components and inflammatory mediators involved in the transmigration of HTLV-1-infected cells across the blood–brain barrier (BBB) are not fully understood. This study proposes a BBB model to identify the immunological mechanisms associated with HTLV-1 pathogenesis. PBMCs from individuals with HTLV-1-associated Myelopathy/Tropical Spastic [...] Read more.
Cellular components and inflammatory mediators involved in the transmigration of HTLV-1-infected cells across the blood–brain barrier (BBB) are not fully understood. This study proposes a BBB model to identify the immunological mechanisms associated with HTLV-1 pathogenesis. PBMCs from individuals with HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) (n = 4) or HTLV-1-infected individuals without HAM/TSP (n = 4) were isolated. An indirect cell co-culture was performed between human brain microvascular endothelial (hBMEC) cells and neuroblastoma (SH-SY5Y) cells. PBMCs from healthy individuals (n = 4) were used as a negative control, and MT-2 cells were used as a positive control. Supernatants and cells were collected to quantify inflammatory cytokines and assess cell death after 24, 48, and 72 h. Multiple comparisons were performed using the Kruskal–Wallis test, followed by Fisher’s LSD post hoc analysis. We observed that the production of cytokines IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, as well as the rate of neuronal death, was higher in co-cultures mimicking HAM/TSP carriers compared to HTLV-1-infected individuals without HAM/TSP and controls. Our results suggest that the HAM/TSP condition induces the release of IL-6, IL-8, IL-1β, TNF, IL-10, and IL-12p70, along with the infiltration of mononuclear cells, which may lead to neuronal death. Full article
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