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Researchers from the Westmead Institute for Medical Research (WIMR) and ���������¼� Sydney have uncovered how the herpes virus spreads through the eye, and how it can be stopped.  

The findings, published in , could pave the way for improved treatments and vaccines for herpes simplex keratitis – the name for when the infection occurs in the cornea.

Approximately , including 40,000 new cases that result in severe visual impairment, and some cases can lead to the need for corneal transplants. Yet little has been known about how the herpes simplex virus type 1 (HSV-1) enters the cornea, or how it spreads, until now.

Researchers developed a new model in the lab to examine the earliest stages of infection, said WIMR’s They used a highly sensitive method for detecting HSV DNA, RNAscope (the ability to look at single RNA molecules) and fluorescently labelled virus. The project was the first HSV-1 study to use RNAscope. 

“To examine the initial infection and spread of HSV-1 in detail, we adapted a model developed at WIMR and previously used to map viral infection in human genital mucosa,” said Prof. Cunningham.

“We discovered that for HSV-1 to enter the cornea, there must be some existing trauma to the uppermost layer of the epithelium, allowing the virus to enter."

The cornea comprises three main layers – the epithelium, stroma and endothelium. The anterior limiting membrane (ALM) or Bowman’s layer sits between the epithelium and stroma.

“Interestingly, while the HSV-1 virus spreads quickly, we observed that it remained in the epithelium layer and did not penetrate the Bowman’s layer,” said Prof. Cunningham.

“So, while the virus can spread and cause significant damage to sight, it is contained within the epithelium. This means that the design of new effective treatments and vaccines for herpes keratitis must take into account how quickly the virus spreads.”

The researchers also identified the presence of a protein called SPRR1A – known to contribute to the protective barrier function of skin – in the uppermost epithelium layer. It was also found in Bowman’s layer when the cornea was infected.

“Its presence in the cornea suggests that this barrier function contributes to limiting both superficial and deep HSV-1 spread,” said Prof. Cunningham. 

Joint lead investigator, Associate Professor Nicole Carnt, from ���������¼�'s School of Optometry and Vision Science and WIMR’s Centre for Vision Research, said the findings were key to improving treatments for the vision-threatening eye infection, which currently has no cure.  

“The virus hides in the trigeminal ganglion of the brain and can reactivate in the eye with no warning,” A/Prof. Carnt said.

“This study reveals the cornea's impressive defenses against HSV1-related scarring and vision loss. Beyond aiding vaccine development, it identifies gene targets to enhance these protective mechanisms in keratitis patients.”

“These breakthroughs are key to preventing recurrence, as well as initial disease and improving patients’ lives."

The research team is now using this model to examine donated human corneas from patients undergoing corneal transplant for blindness caused by herpes simplex keratitis.  

The next phase will aim to discover why some people with herpes simplex keratitis develop scarring and blindness, while others do not.

A/Prof. Carnt added the research approach could also help uncover critical insights into other serious eye infections, such as Acanthamoeba keratitis — a rare but potentially blinding condition often linked to contact lens use.