Anna Cliffe

Publications

• Key questions on the epigenetics of herpes simplex virus latency
• Ex Vivo Herpes Simplex Virus Reactivation Involves a DLK-Dependent Wave of Lytic Gene Expression that is Independent of Histone Demethylase Activity and Viral Genome Synthesis
• DLK-Dependent Biphasic Reactivation of Herpes Simplex Virus Latency Established in the Absence of Antivirals
• The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome
• Ex Vivo Herpes Simplex Virus Reactivation Involves a Dual Leucine Zipper Kinase-Dependent Wave of Lytic Gene Expression That Is Independent of Histone Demethylase Activity and Viral Genome Synthesis
• c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation
• Reactivation of Herpes Simplex Virus (HSV) from Latency in Response to Neuronal Hyperexcitability
• Restarting Lytic Gene Transcription at the Onset of Herpes Simplex Virus Reactivation
• De Novo Polycomb Recruitment: Lessons from Latent Herpesviruses
• PML‐NB‐dependent type I interferon memory results in a restricted form of HSV latency
• De Novo Polycomb Recruitment: Lessons from Latent Herpesviruses
• c-Jun signaling during initial HSV-1 infection modulates latency to enhance later reactivation in addition to directly promoting the progression to full reactivation
• Co-option of mitochondrial nucleic acid sensing pathways by HSV-1 UL12.5 for reactivation from latent Infection
• Neuronal hyperexcitability is a DLK-dependent trigger of HSV-1 reactivation that can be induced by IL-1
• PML-Dependent Memory of Type I Interferon Treatment Results in a Restricted Form of HSV Latency
• Physiological oxygen concentration during sympathetic primary neuron culture improves neuronal health and reduces HSV-1 reactivation