Anna Ruth Cliffe

The paper develops a human-derived in vitro model of nociceptive signaling using HD10.6 cells to study pain mechanisms and drug responses.

This study shows that H2AK119ub1, deposited by PRC1, is critical for HSV-1 reactivation from latency, while H3K27me3 is not.

This study identifies Daxx-mediated histone H3.3 deposition on HSV-1 DNA as a host restriction factor that limits genome decompaction and immediate-early transcription.

This study shows that interferon-induced H3K9me3 and ATRX restrict HSV-1 reactivation by maintaining epigenetic memory during neuronal latency.

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.