Inflammatory and Neuronal Biomarkers Associated With Retinal Thinning in Pediatric HIV

PURPOSE. The pathophysiology of neuroretinal thinning in children with human immunodeficiency virus (HIV) is poorly understood. The current study aimed to assess whether neuroretinal thinning in clinically stable perinataly HtV-infected children was associated with biomarkers of immune activation, inflammation, and neuronal damage. METHODS. Inflammation-associated and neuronal damage markers were measured in blood and cerebrospinal fluid (CSF) of HIV-infected children aged 8 to 18 years. Using mixed-effects regression analyses, we assessed associations between these biomarkers and neuroretinal layer thickness, as measured with spectral-domain optical coherence tomography. RESULTS. Thirty-two HtV-infected children (median age 13.6 years, 50% male) were included. Blood plasma levels of interleukin-6, monocyte chemoattractant protein-i, and soluble intercellular adhesion molecule-1 were inversely correlated with foveal inner plexiform layer thickness (coef= -4.40, P <0.001; coef = -9.67, P = 0.047; coef= -10.48, P = 0.042, respectively). Plasma interleukin-6 was inversely correlated with foveal ganglion cell layer thickness (coef = -2.49, P = 0.010). Total Tan levels in CSF were inversely correlated with outer nuclear layer and inner segments thickness (foveal: coef = -19.3, P = 0.029; pericentral: coef 18.09, P = 0.006) and pericentral total retinal thickness (coef= -28.2, P = 0.017). CONCLUSIONS. Neuroretinal thinning was associated with inflammation-associated and neuronal injury biomarkers in a cohort of antiretroviral therapy-treated perinatally HWV-infected children. These findings suggest that ongoing immune activation, inflammation, and neuronal injury occur in parallel with retinal thinning in pediatric HV