In a paper published in Cell Host and Microbe, Anna Cliffe, a postdoctoral fellow in Deshmukh lab, identifies how activation of JNK in response to neuronal stress triggers changes to the HSV chromatin and reactivation from latency.
![image2](https://www.med.unc.edu/neuroscience/wp-content/uploads/sites/782/2018/07/deshmukh-lab-discovers-the-role-of-a-neuronal-stress-pathway-in-triggering-herpes-simplex-virus-hsv-reactivation-image2-226x300.jpeg)
![image3](https://www.med.unc.edu/neuroscience/wp-content/uploads/sites/782/2018/07/deshmukh-lab-discovers-the-role-of-a-neuronal-stress-pathway-in-triggering-herpes-simplex-virus-hsv-reactivation-image3.jpeg)
In a paper published in Cell Host and Microbe, Anna Cliffe identifies how activation of JNK in response to neuronal stress triggers changes to the HSV chromatin and reactivation from latency. While stress is generally considered to be a factor that triggers HSV reactivation from latency, the molecular mechanisms were unknown. Cliffe et al. show that a neuronal stress pathway involving JNK activation is crucial for HSV reactivation. They found that JNK signaling induces histone phosphorylation on repressed viral promoters, therefore linking cell stress with initial stimulation of viral gene expression.
For more information, visit the the press release and the paper.