Post-mortem PD brains have demonstrated co-localization of EBV markers with α-syn aggregates and evidence of aberrant neuronal cell cycle reentry, suggesting that EBV may drive neurodegeneration through mitotic catastrophe.120 In addition, persistent EBV infection activates pro-inflammatory pathways and the subsequent release of IL-1β, IL-6, TNF-α, and C-reactive protein (CRP), thus increasing the risk of PD.123,124. The gene discussed is CRP; the disease is Epstein-Barr virus infection.