Most cells in the human body have a self-destruct trigger. A protein called RIPK3 activates cell death in the event of certain infections or other types of cell damage. This is a protective mechanism to prevent pathogens, like viruses, from using the cell’s biological apparatus to survive, thrive and spread. But new research shows that brain cells or neurons behave differently and do not “commit suicide” when under attack.
Researchers at the University of Washington School of Medicine conducting mouse studies on West Nile virus infections have found that activation of RIPK3 in neurons does not activate cell death because signaling in the central nervous system is different from other parts of the body. Instead, the protein is part of signaling system that activates anti-viral inflammation in the body.
When the West Nile virus infects the brain, RIPK3 responds by signaling the manufacture of chemokines, which in turn summon the immune system’s white blood cells to the site of infection. These white blood cells flush the brain of the virus. RIPK3 does not trigger neuron death and does not prevent the virus from preporducing inside the neuron but restricts the infection.
The implications of this research, published in the journal Cell, lies in the development of drugs to control RIPK3 while trying to treat certain neurological conditions. The authors of the paper note that interfering with RIPK3 could make the brain susceptible to viral infections.
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