Targeting Metabolic Pathways to Combat Epstein-Barr Virus Infections
The Epstein-Barr virus (EBV) is a pervasive pathogen that infects over 90% of the world’s population, typically without causing any symptoms. However, in some individuals, EBV can lead to a spectrum of diseases, including certain types of cancer and autoimmune conditions. Despite its prevalence, there is currently no specific treatment or vaccine to target EBV.
Recent research from the University of Basel has shed light on how EBV hijacks the metabolism of infected cells, potentially opening up new avenues for therapeutic intervention.
EBV Hijacks Cell Metabolism
The study, published in the journal Science, revealed that EBV infection triggers the upregulation of an enzyme called indoleamine dioxygenase-1 (IDO1) in infected B cells. This enzyme is involved in the production of an energy molecule called NAD+, which is essential for the survival and proliferation of EBV-infected cells.
By manipulating the cell’s metabolism in this way, EBV creates an environment that supports its own growth and evasion from the immune system.
Potential Treatment Approach
The researchers found that inhibiting IDO1 activity with drugs that had previously failed in cancer trials could effectively reduce the transformation of B cells and curb the progression of EBV-associated disease in animal models.
“This finding suggests that a second chance may be given to this class of drugs to treat EBV infections and prevent related diseases,” said Christoph Hess, the study’s lead author.
Clinical Implications
The study’s findings could have significant clinical implications, particularly for individuals who are at high risk of developing EBV-related complications, such as transplant patients and individuals with weakened immune systems. By monitoring IDO1 levels in these patients, it may be possible to identify those who are at risk of developing EBV-associated disease and intervene early on.
Future Research Directions
The researchers emphasize that further research is needed to validate their findings in larger clinical studies and to investigate the long-term effects of IDO1 inhibition in EBV-infected individuals. They also plan to explore the role of IDO1 in other EBV-associated diseases, such as autoimmune disorders.
Conclusion
The study by Hess and his colleagues provides valuable insights into the metabolic reprogramming caused by EBV infection. By identifying IDO1 as a potential therapeutic target, their findings offer a promising avenue for the development of new treatments to combat EBV-associated diseases.
Deepika 
Divya