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This could in part be due to the lower levels of ApoE in the CNS of ApoE4 carriers (Flowers and Rebeck, 2020), thus offering less overall antimicrobial protection, but also mechanistically as ApoE4 prevents HSV-1 cellular attachment but crucially not viral entry or replication, and can also be incorporated into the HSV-1 virion that can enhance release from the cell (Feng et al., 2023), which would be an issue for viral AD

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