广东专家在《自然》发表EB病毒感染机制突破性发现

Core Findings - The research team from Sun Yat-sen University has made a significant breakthrough in understanding the infection mechanism of Epstein-Barr Virus (EBV), identifying R9AP as a universal key receptor for EBV infection in both B lymphocytes and epithelial cells, challenging the traditional view that these cells use different receptors for infection [4][5]. - Over 95% of the global population is infected with EBV, which is associated with various diseases, including infectious mononucleosis, multiple sclerosis, chronic active EBV infection, autoimmune diseases, and several types of cancers [4]. Group 1 - The study established an efficient EBV infection model and discovered that R9AP plays a crucial role in the infection process of both B lymphocytes and epithelial cells, overturning the previous belief that distinct receptors were used for each cell type [4][5]. - Previous research identified key receptors for EBV infection in B cells, such as CD21 and HLA-II, but the mechanism for epithelial cell infection remained unclear until this study [4]. - The research demonstrated that silencing or knocking out R9AP significantly inhibits EBV infection, while increasing R9AP levels promotes infection, confirming its critical role in the infection process [5]. Group 2 - The study revealed that R9AP is not only present in retinal photoreceptor cells but also in peripheral blood/tonsil B cells, various epithelial cells, and EBV-related tumor cells, expanding the understanding of R9AP's biological functions [5]. - The research confirmed the direct interaction between R9AP and the gH/gL complex, highlighting its essential role in the fusion process, which provides a solid molecular target for developing effective and broad-spectrum anti-EBV drugs and vaccines [5]. - The research effort spanned over ten years, with significant advancements made in response to peer review feedback, culminating in the identification of a potent monoclonal antibody that can block EBV infection [6].