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Breaking bad mitochondria
Date:4/15/2014

e amino acids and lipids from the catabolized mitochondrion) to help fuel its continued replication and virulence.

"It's like the bad part of the house is demolished to the benefit of the virus," Siddiqui said.

In their experiments, the researchers showed that hepatitis C-infected cells with higher Drp 1 protein levels also produced less interferon, the body's natural immune booster. These cells were also less likely to undergo apoptosis, a process that would encourage damaged cells to essentially kill themselves.

The reverse was also observed: When the Drp 1 protein was "silenced," interferon production and apoptotic activity increased.

"Mitochondrial processes are at the center of understanding the persistence of the virus and how it flies under the radar of the body's natural immune response," he said. "The trick is to find a way to deliver a drug that could target the Drp 1 protein specifically in hepatitis C-infected liver cells, maybe through nanotechnology."


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Contact: Scott LaFee
slafee@ucsd.edu
619-543-6163
University of California - San Diego
Source:Eurekalert  

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