Researchers have finally figured out how herpes reactivates when we—and our neurons—are stressed out. They also uncovered how brain cells are duped into allowing bits of virus to escape.
About 90 percent of the US population has the herpes simplex virus (HSV), which leads to cold sores, eye infections, genital lesions, and, in rare cases, inflammation of the brain. The closely related varicella zoster virus also causes chicken pox and shingles.
“The proteins we’ve shown to be important for viral reactivation are almost exclusively found in neurons, so they do represent a good therapeutic target,” says virologist Anna Cliffe, first and co-corresponding author of the study and a postdoctoral fellow in the department of cell biology and physiology at the University of North Carolina School of Medicine.
This research, conducted in the lab of UNC’s Mohanish Deshmukh and published in the journal Cell Host and Microbe, was accomplished using primary neurons from mice. But the researchers say the cellular pathways involved are found in human neurons.
Herpes Can Sense Stress
Earlier research suggested HSV stayed dormant in neurons. Deshmukh’s expertise is in neuron survival and death. He wondered if HSV “chooses” neurons as hosts because brain cells are survivors; unlike other cell types, neurons are very wary of triggering cell death even if infected by a virus.
Cliffe’s expertise as a virologist allowed Deshmukh’s team to investigate how HSV reactivates in neurons. As a first step, Deshmukh and Cliffe figured out how to force the virus to go latent in mouse primary neurons in a dish and then to become reactivated. This allowed them to study specific cellular proteins that they suspected are involved in viral reactivation.
