After a group of scientists discovered that the Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) can infect and multiply in human neurons, as previously reported by HNGN, a new team of University of North Carolina Health Care researchers have released a study that sheds light on the cellular mechanism in neurons that reactivates the virus and allows it to escape neurons and stimulate disease.
"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," Anna Cliffe, first author of the study, said in a press release. "We've known that stress triggers viral reactivation. What we've now found is how stress at the cellular level allows for viral reactivation."
The researchers found that a pathway related to JNK, a protein linked to stress, as well as the DLK and JIP3 proteins, was activated just before the herpes virus began to leave mouse neurons.
"We then used a chemical inhibitor to block the JNK pathway to see if that stopped viral reactivation," said Mohanish Deshmukh, senior author of the paper. "And it had a spectacular effect. When we inhibited JNK, the virus was no longer able to reactivate."
Although the research examined the primary neurons in mice, the cellular pathways examined and involved in the process of herpes reactivation are also found in human neurons.
"We're excited about the possibility that this stress-activation pathway exists in humans," said Deshmukh, senior author of the paper. "All of the elements of these pathways are found in human neurons. And we know that stress reactivates herpes simplex virus in humans."
