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Updated: Jul 12, 2026

Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
Published on: January 5, 2016
HIV-1 upregulates intercellular adhesion molecule-1 gene expression in lymphoid tissue of patients with chronic HIV-1
Marta Garrido1, Anna Mozos, Antonio Martínez
1Department of Pathology, Hospital Clínic, Institut d'Investigacions Biomédiques August Pi i Sunyer, University of Barcelona, Barcelona, Spain.
Objectives:
Intercellular adhesion molecule (ICAM)-1 is an adhesion molecule that plays an important role in the transmission of HIV-1 to CD4+ target cells and in the decrease of these cells in lymphoid tissue (LT). Our main objective was to study ICAM-1 expression in LT from HIV-1-infected persons and to correlate this expression with LT viral load and the immunoarchitecture alteration before and after highly active antiretroviral therapy (HAART).
Methods:
Tonsillar LT samples from 16 patients with chronic asymptomatic HIV-1 infection were studied before initiating treatment and after 12 months of HAART. ICAM-1 protein expression was studied by immunohistochemistry in all cases, and ICAM-1 messenger RNA (mRNA) was quantified from frozen tissue in 6 patients using quantitative real-time polymerase chain reaction (PCR). LT viral load was determined by PCR. The LT immunoarchitecture, p24 immunoexpression, and CD4+ cell count were assessed from tissue sections.
Results:
Before initiating HAART, there was high immunohistochemical ICAM-1 expression in follicular dendritic and endothelial cells and high ICAM-1 mRNA quantification. These findings correlated with a high LT viral load, strong p24 expression, and an effacement of LT immunoarchitecture with a low number of CD4+ cells. After HAART, there was a significant decrease of immunohistochemical and gene ICAM-1 expression. These results correlated with a significant decrease of LT viral load and p24 immunoexpression, a recovery of LT architecture, and a significant increase of CD4+ cells.
Conclusions:
HIV-1 upregulates ICAM-1 expression in LT. This finding is associated with a marked effacement of LT architecture. HAART produces downregulation of ICAM-1 expression and recovery of LT architecture by reducing LT viral load significantly.
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