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OCT et VIH : un œil sur la neuro-dégénérescence associée au VIH

Despite the combined antiretroviral therapy (cART), HIV/NeuroAIDS continues to be a major concern and HIV-associated neurocognitive disorders (HAND) are currently its prominent clinical expression. Although severe HIV-associated dementia has drastically declined, 20–50% of persons living with HIV (PLHs) may develop milder HAND forms. The concept of the retina being an anatomical and functional central nervous system surrogate is increasingly recognized. Therefore our goal was to compare spectral-domain optical coherence tomography (SD-OCT) peripapillary retinal nerve-fiber–layer (pRNFL) thickness, and macular thickness and volume between PLHs with well-controlled infections and age-matched HIV-negative controls.

Concurrent cohort study with HIV-negative controls. Fifity-six PLHs, infected for at least 10 years and with sustained plasma HIV-load (plVL) suppression on cART for at least 5 years, and 56 matched HIV-negative healthy controls (HCs) underwent SD-OCT with thorough ophthalmologic examination, cognitive assessment and brain MRI. Their overall and quadrant pRNFL thicknesses, and macular thicknesses and volumes were compared. Clinical Trial registered at www.clinicaltrials.gov (identifier: NCT02003989).

The median [interquartile range, IQR] ages of PLHs and controls, respectively, were 52 [46–60] and 52 [44–60] years. Respective median [IQR] nadir and current CD4+-cell counts were 249/µl [158–350] and 691/µl [526–1053], with median current CD4/CD8 ratio at 0.95 [0.67–1.10]. The median aviremia duration was 11 [8–14] years. No significant between-group pRNFL thickness, and macular thickness and volume differences were found. The mean (+/- standard deviation) pRNFL thickness was 99.5±9.6µm for PLHs and 99.6±8.3µm for HCs (p=0.96). The mean macular volume was 8.7 ± 0.4 mm³ for PLHs and 8.6 ± 0.4 mm³ for HCs (p=0.52). The mean retinal thickness was 296.1 ± 13.5µm for PLHs and 294.0 ± 14.6µm for HCs (p=0.42).

In our cohort of PLHs infected for a mean of 20 years, cART-treated for 17 years and having sustained aviremia for 11 years, we should have detect a –5µm pRNFL thinning with 90% statistical power. The probability of measuring pRNFL thinning as tiny as –0.1 µm, if the real thinning in PLHs were –5, –4 or –3 µm, was, respectively: 0.1%, 1% or 4.5%. Interestingly, the test–retest variability of SD-OCT–measured pRNFL thickness was ~5 µm. A core of brain-dysregulated processes common to HAND and neurodegenerative diseases was recently advanced. If true, one can expect effects on the pRNFL thickness in HIV/NeuroAIDS similar to those in Alzheimer's Disease, Parkinson's Disease and Multiple Sclerosis. It is unlikely that PLHs could be the unique situation in which neurodegeneration would not affect the SD-OCT–measured pRNFL thickness. More likely, no neurodegeneration occurred in our cohort of well-sustained PLHs.

In conclusion, OCT, a well-established tool to measure pRNFL thinning as an objective and reproducible surrogate marker of neurodegeneration, could not detect neuronal loss within the optic nerve of chronically well-controlled PLHs compared to HCs. That is an optimistic finding in terms of PLH-brain aging.