Cohort study reveals transient blood-brain barrier disruption and altered neurogenesis biomarkers in people with HIV following COVID, suggesting potential mechanisms for persistent neuropathology.
OBJECTIVES: Although acute COVID does not seem to markedly differ by HIV status, the long-term impact of COVID in people with HIV (PWH) remains unclear. METHODS: Samples from 44 participants with or without HIV were obtained approximately 10 days after the initial COVID diagnosis (t = 0) and then 3 (t = 1) and 6 (t = 2) months later. Biomarkers of blood-brain barrier (BBB) and vascular dysfunction, neurogenesis, and inflammatory responses were assessed by multiplex profiling and enzyme-linked immunosorbent assay. RESULTS: The majority of inflammatory biomarkers either decreased or remained unchanged during the evaluated time frame. Notable exceptions were IL-9, TNF-α, and CCL-4, which increased at t = 2 compared with earlier time points. The BBB disruption and vascular dysfunction biomarkers (S100β and soluble Intercellular Adhesion Molecule-1, respectively) increased at t = 1 and then returned to basal levels, suggesting transient loss of BBB integrity. No significant changes were observed between people without HIV and PWH across studied inflammatory and BBB markers. Among biomarkers of neurogenesis, eotaxin/CCL11 was not altered, fibroblast growth factor 2 (FGF-2) was transiently decreased at t = 1 in PWH, and granulocyte colony-stimulating factor was elevated at t = 2 in PWH when compared with the previous time points. CONCLUSIONS: BBB and vascular dysfunction occur after COVID and may be implicated in the development of post-COVID conditions. HIV-1 infection may potentiate post-COVID-induced neuropathology by impairing neurogenesis.
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Adesse et al. (2025) studied this question.
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