How viruses go silent — and how they wake back up.

The Cliffe Lab uncovers the molecular details that underlie how herpes simplex virus hides inside neurons for a lifetime, and the signals that trigger it to reactivate and cause disease.

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Model of HSV-1 latency in neurons: an ATRX and H3K9me3 chromatin block, reinforced by interferon-induced PML/DAXX, restricts viral reactivation.

Interferon strengthens an ATRX·H3K9me3 chromatin block — reinforced by PML/DAXX — that restricts HSV-1 reactivation in latently infected neurons.

Our Focus

Decoding the lifelong dialogue between virus and neuron

Herpes simplex virus infects most of the world's population and persists for life by establishing a silent, latent infection in neurons. We study the chromatin, signaling, and immune mechanisms that keep the virus dormant — and what tips the balance toward reactivation, recurrent disease, and neurological consequences.

Chromatin control of latency

How neurons package the viral genome into heterochromatin — via marks like H3K9me3 and factors such as ATRX and Daxx/H3.3 — to enforce and maintain silencing.

Triggers of reactivation

The neuronal stress and signaling pathways — including DLK/JNK and mitochondrial nucleic-acid sensing co-opted by viral proteins — that awaken the virus from dormancy.

Neuronal innate immunity

How neurons mount and remember antiviral defenses — including interferon-driven immune memory — using human sensory-neuron models to study host–virus conflict.

From the Bench

Latest Publications

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We welcome curious graduate students, rotation students, and postdocs excited about virology, chromatin, and neuroscience. Explore our department and how to apply.

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