The role of host factors in HSV pathogenesis is further elucidated by Bai's identification of ZNF593 as a negative regulator of the cGAS-mediated innate immune response, which attenuates cGAS-DNA binding and subsequently reduces type I interferon production (ref: Bai doi.org/10.1038/s41418-025-01508-5/). This regulatory mechanism is crucial for understanding how HSV manipulates host defenses. Additionally, Koyanagi's research on the UL13 protein of HSV-2 revealed its mimicry of cyclin-dependent kinases, which may influence the regulation of lytic and latent infections, thereby providing insights into the viral life cycle and potential therapeutic targets (ref: Koyanagi doi.org/10.1073/pnas.2500264122/). Collectively, these studies highlight the multifaceted interactions between HSV and host immune mechanisms, emphasizing the need for continued research into targeted therapies that can disrupt these interactions and enhance antiviral responses.