Abstract
After a primary infection, many viruses establish a latent infection and stay invisible for the host immune system until reactivation. To understand how a virus seemingly «under control» could reactivate and induce pathology, it is essential to understand the different cellular mechanisms implicated in the antiviral defense. Promyelocytic leukemia (PML) nuclear bodies (PML-NB) are nuclear relays of the antiviral response implicated in the nucleus-associated intrinsic antiviral defense. Many viruses interfere with the activity of the PML-NB, however not much is known about the capacity of these domains to interact with the nucleus incoming viral genomes. This review describes how a recent study of my team has enabled to decipher, in a physiological context, the role of the PML-NB in the detection, structuration and transcriptional control of the herpes simplex virus 1 (HSV-1). It opens new perspectives to understand how the antiviral response associated with nuclear domains could control many other viruses.
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