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 perinatally HIV-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 HIV-infected children (median age 13.6 years, 50% male) were included. Blood plasma levels of interleukin-6, monocyte chemoattractant protein-1, 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 Tau 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 HIV-infected children. These findings suggest that ongoing immune activation, inflammation, and neuronal injury occur in parallel with retinal thinning in pediatric HIV.