A. R. Cliffe

Single-genome analysis reveals heterogeneous association of the Herpes Simplex Virus genome with H3K27me2 and the reader PHF20L1 following infection of human fibroblasts

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.

c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation

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.

HSV-1 miRNAs are posttranscriptionaly edited in latently infected human ganglia

The paper identifies posttranscriptional A-to-I hyperediting of HSV-1 miR-H2 in latently infected human ganglia, expanding its targeting potential and suggesting a role in regulating viral latency.

DLK-dependent biphasic reactivation of herpes simplex virus latency established in the absence of antivirals

This paper introduces a new HSV-1 reporter virus, Stayput-GFP, to study latency and reactivation in neurons without antivirals, revealing DLK-dependent Phase I reactivation and histone demethylase-dependent Phase II reactivation.

Herpes Simplex Virus Reactivation Induced Ex Vivo Involves a DLK-Dependent but Histone Demethylase-Independent Wave of Lytic Gene Expression

This study shows that HSV-1 reactivation ex vivo involves DLK-dependent but histone demethylase-independent lytic gene expression, preceding infectious virus production.

PML-Dependent Memory of Type I Interferon Treatment Results in a Restricted Form of HSV Latency

This study shows that type I interferon treatment during HSV-1 infection leads to restricted latency by altering viral genome positioning through PML-NBs.

Neuronal Hyperexcitability is a DLK-dependent Trigger of HSV-1 Reactivation that can be Induced by IL-1

This study shows that neuronal hyperexcitability, induced by IL-1β, triggers HSV-1 reactivation through DLK/JNK pathway and histone phosphorylation.