Patryk A. Krakowiak

This study shows HSV-1 UL12.5 promotes reactivation by inducing mitochondrial nucleic acid sensing, which activates innate immune pathways and supports lytic gene expression during latency exit.

This study shows that culturing primary neurons at physiological oxygen levels (5%) improves neuronal health and reduces HSV-1 reactivation without affecting latency establishment.

This study investigates the association of HSV-1 genomes with H3K27me2 and PHF20L1 in fibroblasts, finding that H3K27me2 is linked to genome silencing and that this association is influenced by demethylase activity and transcriptional state.

This study shows c-Jun signaling during HSV-1 initial infection promotes latency and enhances later reactivation by facilitating the transition from Phase I to Phase II reactivation.