Elevated Interferon alpha in plasma but decreased surface Interferon alpha receptor 1 in monocytes from HIV and Alzheimer’s disease patients. 

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Presentation Time: 02:15 PM - 03:30 PM
Poster Board Number: B930
Abstract ID: 5769

Presenting Author:
Yisel Cantres-Rosario , Assistant Professor at Univ. de Puerto Rico Recinto de Ciencias Méd.

Abstract:

People with HIV (PWH) develop HIV-associated neurocognitive disorders marked by infiltrated monocytes, inflammation, and neuronal dysfunction. Despite effective antiretroviral therapy, there is no treatment for cognitive decline. Type 1 interferon (IFN-1) signaling is important for synaptic plasticity and cognitive function. We hypothesized that disrupted IFN-1 signaling triggers monocyte infiltration and cognitive decline. Plasma IFN-alpha (IFN-a) and beta (IFN-b) levels were measured in HIV-negative, PWH stratified by cognitive status, and Alzheimer’s disease (AD) patients by ELISA. IFN-a receptor 1 (IFNAR1) levels in blood mononuclear cells were measured by flow cytometry. IFNAR1 levels in post-mortem human brain tissues of PWH were measured by immunofluorescence. Cognitive impaired PWH showed slightly elevated plasma IFN-a1 levels, while AD patients had significantly higher levels (p=0.03) compared to HIV-negative. Plasma IFN-b significantly decreased in men and women with HIV (p=0.001). A lower percentage of IFNAR1+CD14+ monocytes was detected in PWH (p=0.02) and AD patients (p=0.01), which was significantly lower in men (p=0.03) but not in women. However, IFNAR1 levels were similar in brain tissues. Disrupted IFN-1 signaling may contribute to monocyte phenotype shifts, recruitment to the brain and neurodegeneration. Differential IFN-a and IFN-b plasma levels and biological sex differences warrant further investigation for future diagnostic and therapeutic approaches.