Herpes simplex virus type 1 (HSV-1) infections are a significant global health concern due to the virus's ability to evade apoptosis and establish lifelong latency in the peripheral nervous system. The specific viral components responsible for these effects remain unclear, necessitating individual examination of their molecular impacts. This study focused on investigating the effects of recombinant HSV-1 glycoprotein D (HSV-1 gD), a viral protein essential for host cell entry, and/or aluminum hydroxide, a known neurotoxic agent, on reactive oxygen species (ROS) production, apoptotic markers, and epigenetic modifications in SH-SY5Y neuroblastoma cells. Using inhibitory concentration 20 (IC