This photomicrograph depicts leukemia cells that contain Epstein Barr virus using a FA staining technique. Epstein-Barr virus, EBV, is a member of the Herpes virus family, and is one of the most common human viruses. Image courtesy of the CDC.

Hufeng Zhou, recent recipient of a Leukemia and Lymphoma Society fellowship, and colleagues in BWH’s Infectious Disease Division of the Channing Laboratory have investigated the causal link between the Epstein-Barr virus (EBV) and B-cell lymphomas, identifying so-called “super-enhancers” as key players in the growth of malignant lymphoblastoid cells. The results of their work appear in Cell Host & Microbe.

The Epstein-Barr virus, a human tumor virus discovered 50 years ago, has been tied to multiple forms of cancer including Burkitt’s lymphoma, Hodgkin’s lymphoma and more. The virus, which finds its way to the B cell compartment upon infection, establishes a lifelong infection within its host. Immunocompromising conditions – such as HIV and organ transplantation – can allow EBV-infected B cells to grow uncontrollably, leading to cancer, but the exact mechanism by which cancer-causing genes are activated has been unknown.

Super-enhancers are a class of powerful transcription activators that have been increasingly implicated in cell growth and development, and in the development of cancer. The authors found that EBV cancer-promoting proteins can assemble super-enhancers to drive expression of key genes that play a role in cancer.

“This work represents the first identification of a virus using super-enhancers to alter the host-pathogen relationship,” said Benjamin Gewurz, MD,PhD, an Assistant Professor in the Infectious Disease Division and Bo Zhao, MD, PhD, Instructor in Medicine. “Since super-enhancers are particularly sensitive to chemical inhibition, our study suggests a novel therapeutic target in the treatment of EBV-associated malignancies.”