Understanding How the Epstein-Barr Virus Facilitates Its Spread in the Body

The Epstein-Barr virus (EBV), a common herpesvirus infecting a significant portion of the population, often remains unnoticed in many individuals. While it is usually dormant after initial infection, EBV has the potential to contribute to various health issues, including certain cancers, multiple sclerosis (MS), and other autoimmune disorders.

Recent research conducted by scientists at the German Cancer Research Center (DKFZ) and Heidelberg University Hospital has shed light on how EBV enhances its dissemination within the human body. The study found that EBV-infected immune cells, particularly B cells, acquire increased mobility, enabling the virus to spread more effectively. This migration ability is crucial, as it facilitates the distribution of the virus across different tissues, potentially leading to disease development.

EBV is the first virus confirmed to be carcinogenic in humans, with its role in cancers such as Burkitt's lymphoma and stomach cancer well-documented. The interactions between EBV and the immune system are complex; the virus manipulates immune cells to favor its survival and spread. Furthermore, these interactions appear to influence the onset of autoimmune diseases, where immune cells mistakenly attack the body's own tissues, as seen in MS, where myelin sheaths of nerve cells are targeted.

In Germany, over 95% of adults over 50 carry EBV, typically contracted during childhood without symptoms. When infections occur later in life, they often cause Pfeiffer’s glandular fever, characterized by swollen lymph nodes and sore throat. The virus persists in a dormant state in most individuals, but in some, it can reactivate and contribute to tumor formation or autoimmune reactions.

EBV specifically targets B cells, which are central to immune responses. These infected B cells can multiply uncontrollably, leading to lymphomas, or invade the nervous system, contributing to MS. Recent discoveries highlight that EBV influences how B cells migrate through the body. The virus produces proteins such as EBNA2 and LMP1, which increase the production of cytokines like CCL4, promoting B cell movement and invasion into tissues like the brain.

An important breakthrough from DKFZ researchers involves understanding the 'homing' behavior of infected B cells. Homing allows immune cells to migrate from lymphatic vessels to specific tissues to combat pathogens. EBV manipulates this system by enabling infected B cells to overcome barriers of blood vessel walls, facilitated by cytokines and receptors like CCR1. This migration leads to widespread distribution of the virus and increases the risk of disease.

The team identified two viral proteins that trigger this behavior, suggesting potential targets for therapy. Blocking these proteins could prevent B cells from spreading the virus, offering new strategies to treat or prevent EBV-related diseases, including MS and certain cancers. Experiments in animal models using inhibitors to interfere with B cell migration have shown promising results in reducing viral spread.

This research opens the door to developing targeted therapies that could halt the movement of EBV-infected B cells, potentially preventing the progression of associated autoimmune diseases and cancers. Further studies are needed to confirm if these approaches are effective in humans, paving the way for novel treatments against EBV-related health conditions.

For more detailed information, see the original study: Susanne Delecluse et al, "Epstein–Barr virus induces aberrant B cell migration and diapedesis via FAK-dependent chemotaxis pathways," Nature Communications (2025).