New Drug May Stop Cancer-Causing Epstein-Barr Virus

Researchers at Duke University have found that the drug rapamycin may be effective at controlling cell division of B cells infected with the Epstein-Barr virus. The research paper based on the discoveries made by the Duke scientists will be published in the journal, Proceedings of the National Academy of Sciences.

It’s estimated that nine out of every ten adults across the world are carriers of the Epstein-Barr virus, which is capable of inducing cancer in some. The Epstein-Barr virus – like all other viruses – is dependent on host cell machinery to replicate. Cells infected with the virus will often begin to divide more rapidly, and may even begin to break down cellular components in order to free up amino acids, nucleotides and lipids.

The Epstein-Barr virus infects a type of white blood cell – known as a B cell – which is important in immune system function. According to the Duke University Researchers, once the infected B cells begin to run out of those building blocks necessary for cell division and viral replication, they enter a phase known as “cell senescence.”

This senescent state causes the B cells to cease division, which also prevents the Epstein-Barr virus from replicating and infecting adjacent cells. Michael Anthony Epstein and Yvonne Barr were to first to identify the virus’s carcinogenic effects on human tissue.

While the immune system is often sufficient to prevent widespread infection and potentially cancer-causing cellular damage by the Epstein-Barr virus, immunocompromised individuals are still at risk of developing cancer caused by the virus. Epstein-Barr is often the cause of lymphomas and other cancer types in individuals receiving immunosuppressant drugs following an organ transplant.

Micah Luftig, associate professor of molecular genetics and microbiology in the Duke School of Medicine and lead author of the new study, wondered if replication of the Epstein-Barr virus could be induced by triggering the cell’s senescence response. Luftig and his colleagues found that the Epstein-Barr virus was able to influence the cell’s metabolism by manipulating the cell to use any internal fuel source to keep dividing, thereby preventing the B cells from entering a senescent state.

The researchers decided to introduce the drug rapamycin to the infected cells, in order to trick them into thinking they were running out of the building blocks necessary for cell division. They found that the drug was effective at inducing the senescence response, which could potentially be used to halt the spread of the Epstein-Barr virus in patients with compromised immune systems.