New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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Drug shows promise for halting cancer virus via EBV Suppression

Discussion in 'Other Health News and Research' started by Ecoclimber, Jan 20, 2016.

  1. Ecoclimber

    Ecoclimber Senior Member


    Drug shows promise for halting cancer virus

    Written by Catharine Paddock PhD

    Nine out of 10 adults worldwide carry the Epstein-Barr virus, which causes cancer in a small minority of those infected. Now, a new study suggests the drug rapamycin may offer a way to control the virus.


    Green fluorescent dyes in this microscopic view mark the presence of the glucose transporter, GLUT1, on the surface of lymphoblastoid cells which go on to form the lymphomas caused by Epstein-Barr virus. GLUT1 appears here because these cells have been taken over by the virus, which increases demand for more glucose to continue its infectious path. (Amy Hafez, Duke University) Permissions (all or registered reporters) All Usage restrictions (if any) None

    The researchers found they could use the drug rapamycin to make B cells - a type of white blood cell - infected with the Epstein-Barr virus go in and out of a state where they stop dividing.

    The study - from Duke University in Durham, NC - is about to be published in the Proceedings of the National Academy of Sciences.

    A virus spreads by entering cells and redirecting their machinery to make copies of itself. To satisfy a sudden increase in demand, the rapidly dividing host cells will even recycle their own insides to free up building blocks like amino acids, fats and nucleotides.

    The Epstein-Barr virus exerts this effect on B cells - a type of white blood cell in the immune system. But the Duke scientists observed that when the host cells begin to run out of materials, they enter a suspended state called "cell senescence."

    When the B cells are in the senescent state, they stop dividing, which also freezes progress of the Epstein-Barr virus infection.

    Epstein-Barr was the first virus shown to cause cancer in humans. Michael Anthony Epstein and Yvonne Barr discovered it in cell lines cultured from tumor tissue taken from a Burkitt lymphoma over 50 years ago.
    The virus can cause lymphomas and other cancers - mostly in people with weakened immune systems, for instance if they are receiving treatments that suppress the immune system, perhaps following an organ transplant.
    Rapamycin turns senescence on and off in infected cells

    Micah Luftig, lead author of the new study and associate professor of molecular genetics and microbiology in the Duke School of Medicine, says that in most cases, the immune system stops the Epstein-Barr virus making much progress; but he and his colleagues wondered if there could be another route - through the newly discovered senescence trigger.

    With the help of new techniques that allow them to see what state each cell is in, the team could see differences from one cell to the next in the type of viral gene activity that was going on.

    They discovered that the Epstein-Barr virus was able to direct cells to another fuel source to keep them dividing as they digested their own internal parts to free up more building blocks.

    This meant that the infected B cells were somehow not able to enter the senescent state. Perhaps there was a way to trigger them to do this, the team wondered. So they tried to make the cells sense they were running out of materials by using the drug rapamycin.

    The team found that using rapamycin, they could turn senescence on and off in cells infected with Epstein-Barr virus.

    Rapamycin has other curious effects. For example, in 2012, Medical News Today reported on a study where scientists at the Dana-Farber Cancer Institute discovered why some patients who received rapamycin developed diabetes-like symptoms. Their experiments on mice showed that the drug led to a drop in insulin signaling that was triggered by a protein called YY1.

    Duke University news release, accessed 20 January 2016.
    Bob, leela and Theodore like this.

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