Age-related macular degeneration (AMD) is a neurodegenerative disease affecting the retina, and the leading cause of vision loss in the elderly in developed countries. Although several risk factors have been identified, the factors triggering the disease are still not fully understood.
Among existing hypotheses, a role for cytomegalovirus (CMV) (a member of the herpes virus family) in the onset and/or progression of AMD has been suggested. A post-mortem study showed that the posterior part of the eye could be a relatively common site of CMV latency in the general population. Furthermore, according to some in vitro and animal studies, CMV may participate in the onset/progression of AMD via pro-inflammatory and/or pro-angiogenic mechanisms.
Nevertheless, the impact of CMV on AMD remains largely unstudied in humans: only one small cross-sectional study has explored this association, showing a link between high levels of anti-CMV antibodies and neovascular AMD. However, determining whether CMV contributes to AMD onset or progression of AMD is essential, given the potential implications for treatment and prevention (antiviral therapies).
Using data from over 1,000 UK Biobank participants, we aim to assess whether CMV infection (estimated via anti-CMV plasma serology data) is associated with retinal layers thicknesses (measured by optical coherence tomography (OCT)). A particular focus will be given to the photoreceptor layer and the retinal pigment epithelium-Bruch’s membrane complex, which are known to be affected in AMD. Multivariate linear regression models will be performed to account for potential confounding factors. Moreover, thanks to the availability of genetic data in a subsample of participants, we will conduct stratified analyses on a genetic risk score for AMD to assess whether genetic background could modulate the impact of the virus on the risk of AMD.
