Recent studies have significantly advanced our understanding of the herpes simplex virus type 1 (HSV-1) and its interactions with host cells. A notable contribution is the development of a glycoengineered keratinocyte library, which has elucidated the essential roles of specific glycans throughout the HSV-1 infection cycle. This innovative approach allows for a more nuanced analysis of host-pathogen interactions, highlighting the potential for targeted therapeutic strategies (ref: Bagdonaite doi.org/10.1038/s41467-023-42669-6/). Additionally, a real-world cohort study evaluated the long-term effectiveness of the live zoster vaccine, revealing a significant decline in vaccine efficacy against postherpetic neuralgia and hospital admissions for herpes zoster over a decade. Specifically, the effectiveness waned from 83% to 41% against postherpetic neuralgia, underscoring the need for ongoing monitoring and potential booster strategies (ref: Klein doi.org/10.1136/bmj-2023-076321/). Furthermore, comparative studies on viral-induced anterior uveitis have shown a stronger immune response to HSV-1 than to murine cytomegalovirus, suggesting distinct pathogenic mechanisms that could inform future therapeutic interventions (ref: Li doi.org/10.1167/iovs.64.14.20/). The exploration of guinea pigs as a model for ocular herpes pathophysiology has also revealed that while trifluridine is effective in mitigating ocular disease, oral acyclovir and valacyclovir were ineffective, indicating species-specific responses to antiviral treatments (ref: Yadavalli doi.org/10.1167/iovs.64.14.41/). Overall, these studies collectively enhance our understanding of HSV-1 pathogenesis and treatment.