Latent HSV genomes have memory

Read our latest work from MSTP student Jon Suzich on how type I IFN upon de novo infection results in a more restricted form of HSV latency. We also link this restriction to association of viral genomes with PML nuclear bodies.

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Neuronal hyperexcitability is a DLK-dependent trigger of HSV-1 reactivation that can be induced by IL-1

The latest study from our lab published in eLife describes how HSV-1 reactivation can be induced by conditions that induce neuronal hyperexcitability including exposure IL-1. This study may help explain why HSV undergoes reactivation during fever, psychological stress and following sunburn.

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Neuronal Stress Pathway Mediates a Switch

A neuronal pathway involving activation of c-Jun N-terminal kinase (JNK), common to many stress responses, is essential for initial HSV gene expression during reactivation. JNK-dependent reactivation results in a specific change to the HSV epigenome known as a histone methyl/phospho switch, which can permit gene expression to occur from repressive heterochromatin. This study therefore answer a long-standing question as to how viral gene expression can initiate to trigger HSV reactivation.

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