Inflammatory and Neuronal Biomarkers Associated With Retinal Thinning in Pediatric HIV

Area of Science:

• Ophthalmology and immunology
• Neuroscience and infectious diseases

Background:

• The pathophysiology of neuroretinal thinning in children with human immunodeficiency virus (HIV) remains unclear.
• Understanding these mechanisms is crucial for managing long-term complications in pediatric HIV.

Purpose of the Study:

• To investigate the association between neuroretinal thinning and biomarkers of immune activation, inflammation, and neuronal damage in HIV-infected children.
• To explore potential underlying mechanisms contributing to retinal changes in pediatric HIV.

Main Methods:

• Blood and cerebrospinal fluid (CSF) samples were collected from 32 HIV-infected children (aged 8-18 years).
• Biomarkers of inflammation (e.g., IL-6, MCP-1, sICAM-1) and neuronal damage (Total Tau) were measured.
• Neuroretinal layer thickness was assessed using spectral-domain optical coherence tomography (SD-OCT).
• Mixed-effects regression analyses were used to determine associations between biomarkers and retinal thickness.

Main Results:

• Elevated plasma levels of IL-6, MCP-1, and sICAM-1 were inversely correlated with inner retinal layers (foveal inner plexiform layer).
• Plasma IL-6 also showed an inverse correlation with the foveal ganglion cell layer thickness.
• CSF Total Tau levels were inversely correlated with outer retinal layers (outer nuclear layer, inner segments) and total retinal thickness.

Conclusions:

• Neuroretinal thinning in perinatally HIV-infected children on antiretroviral therapy is associated with inflammation and neuronal injury biomarkers.
• These findings indicate that immune activation, inflammation, and neuronal injury persist and occur alongside retinal thinning in pediatric HIV.
• The study highlights the complex interplay between systemic inflammation, neuronal damage, and ocular health in children living with HIV.