Researchers have discovered molecular and protein signatures that predict rapid onset of liver damage in hepatitis C patients following a liver transplant. The markers appeared soon after transplant and well before clinical evidence of liver damage.
Such early detection of susceptibility to hepatitis C virus-induced liver injury could lead to more personalized monitoring and treatment options after a transplant. Also, because the markers stem from an underlying pathology occurring at a very basic level, they might reveal why hepatitis C is so clinically variable, and suggest new therapies to protect patients' own livers.
The findings were the cover story of the liver disease journal Hepatology. The molecular and protein markers were found in separate studies, one led by Dr. Angela "Angie" Rasmussen, and the other by Dr. Deborah Diamond, both working in the lab of Dr. Michael Katze, professor of microbiology at the University of Washington. The Katze lab employs systems approaches to studying many viral pathogens, including hepatitis C, HIV, influenza, SARS and Ebola.
Liver failure from chronic hepatitis C infection is the leading reasons for liver organ transplantation surgery worldwide, Rasmussen noted. In almost all cases, the newly transplanted organ quickly becomes infected, because the hepatitis C virus persists in the patient's bloodstream. Virus damage to the transplanted organ is sometimes slow, taking years or decades to progress.
However, in about a third of the cases, she said, leathery, fibrous tissue builds up in the transplanted liver within one to two years. This condition, called cirrhosis, can keep the liver from clearing toxins from the body and can end in liver transplant failure.
Physicians have had no means of sorting out which of their patients might be prone to this complication. They have been awaiting prognostic markers for disease progression and therapy response to allow them
|Contact: Leila Gray|
University of Washington