Researchers discover "universal key" for EBV infection, pave way for novel vaccines

GUANGZHOU, June 23 (Xinhua) -- Chinese scientists have identified a protein molecule that acts as a "universal key" enabling the EB virus (EBV) to infect cells, opening new possibilities for developing effective EBV vaccines.

EBV, one of the most common human herpesviruses, is associated with various diseases, and is the leading cause of nasopharyngeal carcinoma. The virus primarily targets B cells and epithelial cells.

While earlier studies established that EBV enters B cells through two specific receptors, the mechanism behind its infection of epithelial cells remained poorly understood. The prevailing theory suggested EBV employed entirely different receptors to invade these two cell types.

However, new research conducted by Sun Yat-sen University, located in south China's Guangdong Province, has uncovered that a protein called R9AP serves as a common receptor allowing EBV to infect both B cells and epithelial cells. These findings were published on Wednesday in the journal Nature.

"R9AP functions like a universal key -- it unlocks both B cells and epithelial cells, allowing EBV to invade," said Zhong Qian, one of the researchers from Sun Yat-sen University.

The researchers found that when R9AP was hidden through gene silencing or knockout techniques, or when its function was disrupted using antibody drugs, EBV struggled to infect these cells. Conversely, increasing R9AP levels made cells more susceptible to viral entry, akin to "duplicating keys" for easier access.

The study also revealed that R9AP is present in various B cells, epithelial cells and EBV-related cancer cells. Previously believed to operate mainly inside cells, the research showed that R9AP can extend outward from the cell membrane -- directly binding EBV and facilitating its entry.

This discovery challenges the long-standing assumption that EBV uses completely separate receptors for B cells and epithelial cells, said Zeng Musheng, one of the researchers from the university.

It provides a critical foundation for both understanding EBV's infection mechanisms and developing highly effective vaccine targets, Zeng noted.  ■