The unappreciated role of developing B cells in chronic gammaherpesvirus infections

Oncogenic gammaherpesviruses, including human Epstein-Barr virus (EBV), human Kaposi's sarcoma-associated herpesvirus (KSHV), and murine gammaherpesvirus 68 (MHV68), establish lifelong latent infection in circulating B cells and directly contribute to the genesis of a variety of malignancies including B cell lymphoma. The prevailing paradigm for gammaherpesvirus biology holds that these viruses initially infect naïve B cells, then drive infected B cells independent of antigen stimulation through germinal center reactions and into the memory B cell compartment, which serves as a stable latency reservoir.

On September 19, Dr. Yiping Wang published a PLOS Pearls mini-review entitled “The unappreciated role of developing B cells in chronic gammaherpesvirus infections” in PLoS Pathogens, in cooperation with Professor Scott Tibbetts at the University of Florida. They review the recent advancements in the understanding of the roles of developing B cells during gammaherpesvirus infection and disease, and propose a new working model for latency establishment that incorporates developing B cell infection into the textbook paradigm. In addition to infecting naive B cells, gammaherpesviruses can also infect developing B cells in the bone marrow, and then drive infected B cells through normal B cell maturation and differentiation pathways, and finally form memory B cell compartment that stably maintains the latent viral genome.

This work was supported by International Science and Technology Innovation and Cooperation Program of Sichuan Province Key Research and Development Project of China (no. 2024YFHZ0327), and NIH R01CA262902 and P01CA214091.

For more information on this paper, please visit:https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012445.