New Strategy for Epstein-Barr Virus and Related Diseases

The Epstein-Barr virus (EBV) is known to cause a myriad of illnesses, including several types of cancer. Recent discoveries indicate that blocking a specific metabolic pathway in cells infected by EBV can reduce the virus's latent state, thereby lowering the risk of subsequent diseases. This promising development was highlighted by researchers from the University of Basel and the University Hospital Basel in a study published in the journal Science.

Anthony Epstein and Yvonne Barr first identified EBV 60 years ago, and it was the first virus proven to cause cancer in humans. Part of the herpesvirus family, EBV was isolated from tumor tissue and later experiments confirmed its cancer-causing potential.

EBV is widespread, with around 90% of adults carrying the virus. Many are infected as children, often without symptoms, while others contract it during adolescence. Acute infection can lead to glandular fever, also known as "kissing disease," which can incapacitate individuals for several months. Beyond its link to cancer, EBV is also suspected to play a role in autoimmune diseases like multiple sclerosis.

Currently, there are no drugs or vaccines specifically targeting EBV. However, researchers from the University of Basel and University Hospital Basel have identified a promising approach to mitigating EBV's impact. Their findings have been documented in Science.

The research team, led by Professor Christoph Hess, discovered that EBV reprograms immune cells known as B cells through a process called "transformation." This transformation is crucial for the virus to establish a chronic infection, which can eventually lead to cancer. The virus achieves this by increasing the production of an enzyme called IDO1 in the infected cells, which boosts the cells' energy production. This additional energy supports the enhanced metabolism and rapid proliferation of the reprogrammed B cells.

Clinically, the researchers examined patients who developed EBV-triggered blood cancer following organ transplantation. Post-transplant, patients' immune systems are suppressed to prevent organ rejection, which creates a favorable environment for EBV to cause blood cancer, known as post-transplant lymphoma. The study revealed that the enzyme IDO1 is upregulated months before the diagnosis of post-transplant lymphoma, suggesting that it could serve as a biomarker for the disease.

Interestingly, IDO1 inhibitors had previously been developed for cancer treatment but were found ineffective. Nonetheless, these inhibitors might now be repurposed to combat EBV infections and related diseases. Experiments on mice demonstrated that inhibiting IDO1 reduced the transformation of B cells, thereby decreasing the viral load and the development of lymphoma.

Professor Hess notes that while it is common practice to use antiviral drugs for transplant patients, there has been no specific treatment for EBV-associated diseases. The newfound understanding of EBV's metabolic manipulation opens the door to potential therapies that could significantly reduce the virus's impact and associated health risks.