The scientific community may be one step closer to stopping the spread of the herpes virus thanks to new Washington State University research.

Herpes simplex virus type 1 (HSV-1) is the most common cause of oral herpes which causes painful blisters better known as cold sores.

WSU researchers recently published a study in the American Society for Microbiology’s journal mSphere that is the first to identify how one of the virus’ proteins acts as a critical signaler for the virus to succeed in infecting a cell.

Herpes simplex virus type 1 invades the body through the epithelial cells that line human organs, including the skin. Once inside, the attack sequence is launched when a protein on the virus’ surface called glycoprotein C detects a change in the cell’s acidity level.  A second protein called glycoprotein B then initiates the attack on the cell. “We may have identified a novel target for intervention because, in theory, if you can prevent that initial infection, you can avoid the virus,” said Tri Komala Sari, a WSU graduate student in the Department of Veterinary Microbiology and Pathology and the paper’s lead author.

Komala Sari said while the virus was able to invade the cell without glycoprotein C, it was significantly delayed in recognizing the change in acidity levels and it wasn’t as effective in taking over the cell.

Understanding the function of this protein could help researchers learn how to keep the virus from invading a cell or lower its efficiency during infection.

According to the Centers for Disease Control and Prevention, HSV-1, the oral form of herpes, infected 47.8% of Americans ages 14 to 49 from 2015 to 2016. The World Health Organization estimates 3.7 billion people under age 50 (67%) have HSV-1 globally. There is no vaccine for the virus. To make matters worse, many people infected don’t show any symptoms.

“After that initial infection the virus hides. That’s why they say, ‘herpes is forever,’ because once you get that latent infection there is no way back from that,” said Anthony Nicola, the G. Caroline Engle Distinguished Professor of Infectious Diseases and principal investigator on the project.

Nicola said understanding how the virus infects the cell may help uncover ways to stop the virus before it goes into hiding. He noted the herpesvirus is far more complex in structure than other viruses. While the herpes virus has about a dozen proteins on its surface with various functions, HIV and influenza have just two or three proteins.

Komala Sari said there’s still a long way to go in blocking the virus, but this finding could be a target of a vaccine in the future.

“Now we need to know more about how that interaction between these two proteins occurs, when and where,” she said.

The work was funded by a grant from the National Institutes of Health.