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The Epstein-Barr virus (EBV) has been known for 60 years as the first virus proven to cause cancer in humans. Researchers from the University of Basel and the University Hospital Basel discovered that inhibiting a specific metabolic pathway in infected cells can reduce latent infection, thus lowering the risk of developing diseases associated with EBV, including various cancers. Most people are carriers of EBV, with around 90% of adults infected with the virus and experiencing no symptoms or illness. While acute infection can cause glandular fever, EBV is also suspected of being involved in the development of autoimmune diseases such as multiple sclerosis.

Currently, there are no specific drugs or vaccinations approved to target EBV within the body. However, the research group led by Professor Christoph Hess has found a promising strategy to combat EBV. They discovered that the virus causes infected immune cells to increase production of an enzyme called IDO1, leading to elevated energy production by mitochondria in the infected cells. This enhanced energy is needed for the rapid proliferation of B cells reprogrammed by EBV. In patients who developed EBV-triggered blood cancer after organ transplantation, the researchers observed upregulation of IDO1 months before the diagnosis of post-transplant lymphoma.

The researchers also found that IDO1 inhibitors, which were previously developed for treating established cancer but have proved unsuccessful, may be repurposed to target EBV infection. In experiments with mice, IDO1 inhibition using these drugs reduced the transformation of B cells, viral load, and the development of lymphoma. This suggests that these inhibitors could potentially be used to dampen EBV infection and combat EBV-associated diseases in transplant patients. Up until now, there have been no specific treatments available for preventing or treating diseases associated with Epstein-Barr virus.

The discovery of the role of IDO1 in EBV infection provides a new avenue for potential therapeutic interventions. By targeting this specific metabolic pathway, researchers may be able to reduce the risk of developing EBV-associated diseases such as cancer. The identification of biomarkers associated with the upregulation of IDO1 in patients with post-transplant lymphoma could also aid in the development of more effective diagnostic tools. Overall, this research sheds light on a new strategy for combating EBV infection and offers hope for the prevention and treatment of EBV-associated diseases.

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