The research team of Sun Yat sen University Cancer Prevention and Treatment Center published a research result in the international academic journal Nature on the 18th, discovering that a protein molecule is the "universal key" for EB virus infected cells, which is expected to provide an efficient target for the development of new EB virus vaccines. EB virus is a common human herpesvirus closely related to various diseases and is the main pathogenic factor of nasopharyngeal carcinoma. EB virus mainly infects B lymphocytes and epithelial cells. Previous studies have shown that EB virus infection of B lymphocytes mainly relies on two key receptors as "keys" to open the door, but the mechanism of how EB virus infects epithelial cells has not been clear. The traditional view is that EB virus infects these two types of cells using completely different receptors. However, a new study conducted by the team of Zeng Musheng, Deputy Director of the Cancer Prevention and Treatment Center at Sun Yat sen University, and Zhong Qian, a researcher from the Experimental Research Department, found that a protein molecule called "R9AP" is a universal key receptor for the EB virus to infect these two types of cells. It is like a 'universal key' that can open the doors of both B lymphocytes and epithelial cells, allowing the EB virus to enter. ”Zhong Qian said. The research team found that once the key to R9AP is "hidden" through gene silencing or knockout techniques, or a "fake key" is created using derived peptides, and interfered with by antibody drugs, it is difficult for EB virus to infect the above two types of cells. On the contrary, if the level of R9AP is increased, it is equivalent to "having a few more keys", making EB virus infection easier. The study also found that R9AP is present in various B lymphocytes, epithelial cells, and EB virus associated cancer cells. R9AP was previously thought to work inside cells with its head facing inward, but this study found that it can also extend its "head" outside the cell, directly "catching" the EB virus and helping it "open the door" to enter the cell. Zeng Musheng stated that this study overturns the traditional understanding that "B lymphocytes and epithelial cells are infected with the EB virus using completely different receptors," providing a scientific basis for a deeper understanding of the mechanism of EB virus infection and exploring efficient vaccine targets for novel EB viruses. (New Society)