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Glandular fever virus linked to blood cancer

University of Sussex, U.K., scientists have been looking at how the Epstein-Barr virus controls two genes. The genes are MYC (which can drive cancer development when it is altered) and BCL2L11 (a gene that triggers cell death to prevent cancer).

Epstein-Barr virus is one of eight known viruses in the herpes family. The virus is best known as the cause of infectious mononucleosis (glandular fever). Epstein-Barr virus is spread by saliva through:

kissing,
sharing drinks and food,
using the same cups, eating utensils, or toothbrushes,
having contact with toys that children have drooled on.

More seriously, the virus has also been associated with forms of cancer, such as Hodgkin’s lymphoma. It is the cancer connection which is the new research focus.

A team led by Professor Michelle West discovered that the virus controls the MYC and BCL2L11 genes by taking-over ‘enhancer’ DNA regions. These genetic enhancers control genes by affecting DNA. Through this the Epstein-Barr virus can turn on the gene associated with cancer – MYC – and turn off the gene that helps to prevent cancer – the BCL2L11. Through this the virus appear to be able initiate and progress human lymphoma.

The research has identified new enhancers which control the BCL2L11 gene. Here the Epstein-Barr virus prevents control centers from contacting the gene.

The research has found a means to reverse the blocking effect by using a specific drug. This could provide the basis to a new treatment. In a research brief, Professor Michelle West explains: “This is a key step towards uncovering how this common virus which, affects thousands of people every year, causes blood cancer.”

Developing a treatment will not be straightforward because of the complexity of the genetic interactions that help lymphoma cells grow and survive. Nevertheless, the discovery indicates a promising research focus.

The research is published in the journal eLife, in a paper headed “MYCactivation andBCL2L11silencing by a tumor virus through the large-scale reconfiguration of enhancer-promoter hubs.”

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Written By

Dr. Tim Sandle is Digital Journal's Editor-at-Large for science news. Tim specializes in science, technology, environmental, business, and health journalism. He is additionally a practising microbiologist; and an author. He is also interested in history, politics and current affairs.

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