Recent studies on Herpes Simplex Virus type 1 (HSV-1) have unveiled novel mechanisms of viral pathogenesis and potential therapeutic strategies. One significant finding is the demonstration of a viral gene drive that can propagate during HSV-1 infection in mice, suggesting a new avenue for therapeutic applications (ref: Walter doi.org/10.1038/s41467-024-52395-2/). Additionally, HSV-1 has been shown to induce N6-methyladenosine reprogramming by suppressing the METTL14 protein, which enhances its oncolytic activity in glioma cells (ref: Chen doi.org/10.1016/j.celrep.2024.114756/). This indicates that HSV-1 not only evades the host immune response but also manipulates cellular processes to its advantage. Furthermore, research has highlighted the virus's ability to inhibit the phosphorylation of RNA polymerase II, thereby disrupting host gene expression and facilitating viral mRNA transcription (ref: Whisnant doi.org/10.1128/jvi.01178-24/). In the context of antiviral strategies, a drug repurposing screen identified decitabine as a potential antiviral agent against HSV-1, addressing the challenge of resistance to existing treatments (ref: Bautista doi.org/10.1128/spectrum.01754-24/). Lastly, a novel serum collection device, Ser-Col, demonstrated high correlation with standard venipuncture for various infectious markers, including HSV-2, suggesting its utility in clinical diagnostics (ref: Harutyunyan doi.org/10.1016/j.cca.2024.119970/).