Jon’s paper was accepted for publication in EMBO Reports. This work described how type I IFN exposure at the time of initial neuronal infection with HSV results in a form of latency that is more restricted for reactivation. Jon also helped answer a key question in the HSV field on the contribution to PML nuclear bodies to latency. He found that they were not required for the establishment of latency in the model system we use. However, genomes associated with PML-NBs are unable to reactivate. We are continuing Jon’s work to understand how PML-NBs alter the viral epigenome to restrict reactivation. Read the manuscript here, and a commentary on the study here.
August 17, 2021 by email@example.com