Herpes Simplex Virus Type 1 Ocular Infection Triggers Brain Inflammation At Steady State And During Neurodegenerative Disease 9051

Description Herpes simplex virus type 1 (HSV-1) corneal infections are one of the leading causes of infectious blindness in developed countries. Past research has shown that infection of the ocular surface with HSV-1 can infect the brain via the olfactory bulb and the trigeminal ganglion (TG), resulting in an inflammatory immune response within the CNS. Studies have indicated that HSV-1 infection may influence the onset and/or development of Alzheimer’s Disease (AD); however, a causative relationship between HSV-1 and AD has not been defined. In an attempt to establish a causal link between HSV-1 and AD progression, we ocularly infected WT and transgenic mice containing the 5xFAD mutation, which spontaneously develop Alzheimer’s Disease. We monitored inflammatory responses in the brains of infected mice over time and found that myeloid cells upregulate more CD11c when mice are infected with HSV-1 compared to uninfected controls. Notably, 5xFAD mice had a basal level of CD11c expression that was higher than WT controls. These data suggest that brain myeloid cells are more activated in the brains of 5xFAD mice, and that HSV-1 infection enhances the level of activation in these cells. Future studies are aimed at identifying if elevated brain inflammatory responses are due to direct HSV-1 infection of brain tissue and if activated immune cells are localized to various regions of the brain. Funding Sources Supported by NIH R01EY026891; NIH U01EY034711 Topic Categories Neuroimmunology (NEUR)