Herpes simplex virus type 1 (HSV-1) is a significant human pathogen, particularly affecting neonates and immunocompromised individuals. Recent studies have elucidated various mechanisms by which HSV-1 facilitates its infection and pathogenesis. One study demonstrated that the aryl hydrocarbon receptor (AhR) enhances HSV-1 lytic infection by promoting viral gene transcription and increasing the expression of viral receptors. Pharmacological inhibition or knockout of AhR resulted in reduced viral protein expression and infectious progeny, indicating its critical role in viral replication (ref: Huang doi.org/10.3389/fcimb.2025.1548038/). Furthermore, innovative tracking methods using carbon quantum dots have been developed to trace HSV-1 from the skin to the brain, providing insights into how the virus reaches the central nervous system and potentially contributes to neurodegenerative diseases (ref: Feng doi.org/10.1002/adma.202508464/). This tracking approach could lead to better understanding and treatment of HSV-1-related encephalitis and Alzheimer's disease. Additionally, an optogenetic platform has been introduced for discovering compounds that modulate the integrated stress response (ISR), which may have therapeutic implications for viral infections, including HSV (ref: Wong doi.org/10.1016/j.cell.2025.06.024/). Overall, these findings highlight the multifaceted interactions between HSV-1 and host cellular mechanisms, paving the way for novel therapeutic strategies against HSV infections.