RPB-supported Researchers ID Master Molecule behind Corneal Inflammation
RPB-supported researchers at the University of Illinois at Chicago have identified an enzyme present in the cornea that triggers inflammation during and even after a herpes virus infection has cleared. Their results are published in the journal Cell Reports.
The herpes simplex virus-1, or HSV-1, is transmitted through body fluids and infects the mouth and eyes, and is one of the leading causes of blindness. It can be eliminated in the eye using antiviral drugs, but inflammation of the cornea can persist indefinitely, requiring ongoing treatment with steroid-based eye drops.
"We wanted to know why there is still inflammation even after the virus is gone from the eye," said Deepak Shukla, the Marion Schenk Professor of Ophthalmology and professor of microbiology and immunology in the UIC College of Medicine. "We thought that there must be a factor or molecule already in the eye that the virus influences in some way, and that molecule helps tip the balance in the cornea towards inflammation."
Shukla and colleagues looked at human corneal cells infected with HSV-1 and saw that an enzyme called heparanase became significantly upregulated and activated in cells just after infection, and remained upregulated well after the initial infection.
"The active form of heparanase was clearly involved in promoting and sustaining inflammation in the cornea through multiple channels," said Alex Agelidis, a graduate student in the UIC College of Medicine and a co-investigator on the study.
Heparanase may be a key factor in other inflammatory disorders, including dry eye disease, Shukla explained. "A drug that blocks heparanase may represent a novel treatment for long-term inflammation associated with HSV-1 infection as well as other inflammatory disorders of the eye," he said.