A treatment for Epstein Barr (EBV) has moved a step closer as researchers have identified a new potential pathway to target the virus. Scientists at the Wistar Institute have discovered two molecules that can disrupt how EBV expresses itself. Lab tests showed that targeting these proteins can stop EBV from growing. Excitingly, there’s already a drug available that targets the protein and could be used to treat EBV, bringing hope to those who need it.
The Epstein Barr virus is common, appearing in 90% of humans. EBV is harmless and stays dormant within the body for most of us. However, for some, EBV can lead patients to develop life-limiting conditions, including multiple sclerosis and specific types of lymphoma. In addition, EBV can lead to an over-production of B-cells, which can be dangerous for patients with a suppressed immune system, such as those with cancer or those who have recently had a transplant.
To understand how the virus works, scientists at the Wistar Institute used modified DNA sequencing, the same approach used to map the human genome. The DNA sequence provides the internal instructions for how the virus works and spreads. “We identified two cellular proteins that are important to folding the EBV genome,” says co-author Italo Tempera, PhD. “The virus was clever to use the same machinery that regulates the conformation of the human genome to also regulate its own gene expression.”
After analysing the DNA sequence, scientists identified the proteins CTFC and PARP1 as playing a pivotal role in EBV expression. Excitingly, there’s already a drug known as olaparib that targets PARP1, bringing treatment for EBV tantalisingly close for those with EBV lymphomas. Known by the brand name Lynparza, it’s already being used to treat patients with ovarian cancer but could also be used to treat those with EBV.
The insight into the genetic mechanisms of EBV provides a stimulus for the development of new and more effective targeted treatments. “Maybe we can expand the way in which we can use this drug not only to interfere with DNA damage, but we also might interfere with DNA folding and gene expression,” says Tempera. He, and his team, are using these insights as the basis for experiments at the Wistar Institute.
The results are encouraging and could, in the future, provide a lifeline for the millions across the world with EBV; however, there are several hurdles any medication must overcome.
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You can read the full paper, The Three-Dimensional Structure of Epstein-Barr Virus Genome Varies by Latency Type and Is Regulated by PARP1 Enzymatic Activity, here.
