HCV AND POST LIVER TRANSPLANTS

[KIMBERLY]

IF YOU OR A LOVED ONE HAS HAD A LIVER TRANSPLANT WITH HCV AND END STAGE CIRROHIS,ESPECIALLY WITH A HIGH VIRAL LOAD AT TRANSPLANT,KISTEN TO ME!!!THIS IS NOT THE CURE ALL ANSWER[THE NEW LIVER]THE HCV VIRUS WILL MOST LIKELY ATTACK THE NEW LIVER WITHIN 3 MONTHS,SO BE PREPARED

[Doug Shultz]

I must be lucky, its been 1year 5 month post transplant Liver, I to have HCV, went on a treatment plan 7 months after transplant, with in 30 days virai load was at (0), I stay on treatment plan for 6 month, Now at 9 month later still at (0) viral load, I have been bless so far. I have came a long way,and back to work, living life on lifes terms.

[Catherine (Cathy)]

Hello Group: My Name Is Cathy I was given a 2nd chance at life August 30 2008 I also have hepatitis C

I am 1 year 7 months with my Donor Within! My viral load has been running since 72 hours after transplant 37 Million 800 Thousand Something? So far Hepatitis C has not started eating my Donor Within! There isn't any treatment left out there that I haven't already tried! I do not plan on doing any type of treatment unless there is more than a 80 % CURE RATE! I don't have time @ 57 years old with severe neuropathy to be ill doing treatment and that is fine per my Transplant Hepatologist

They no longer go by your viral score yes it is hard for me to change my thinking because I was one of 100 to first know I have Hepatitits C just prior to the test coming out in 1992. At the moment of this post my Liver Numbers are Normal......Life Is Great Pay It Forward

[Catherine (Cathy)]

Hepatitis C Recurs Rapidly after Liver Transplant

When a diseased liver is removed from a patient with hepatitis C, serum HCV levels (HCV RNA) decline quickly and significantly. However, after receiving a healthy liver transplant, HCV levels rebound and can surpass pre-transplant levels within a few days, according to a new study published in the February 2006 issue of Liver Transplantation. The journal is available online via Wiley InterScience.

Hepatitis C is the number one reason for liver transplantation in the US. Unfortunately, the virus always recurs in the new liver. Since mathematical models have been useful in the study of the viral dynamics of HIV and hepatitis B, researchers, led by Kimberly A. Powers and Ruy M. Ribeiro of the Los Alamos National Laboratory in New Mexico, sought to use a mathematical model to quantify the liver reinfection dynamics of HCV.

The researchers, in collaboration with a surgical team lead by John McHutchison now at Duke University Medical Center, followed six HCV-infected patients who received cadaveric liver transplants. They collected blood samples before, during and after transplantation to assess changing levels of HCV RNA that was measured using reverse transcription polymerase chain reaction assay. They then plugged the data into a mathematical model, correcting for fluid balance, and analyzed the results using linear regression.

“In most patients,” the authors report, “HCV RNA levels decreased rapidly during and after transplantation and subsequently began to increase – reaching above pre-transplant levels in all but one patient – within a few days of the procedure.” They found that when the diseased liver was removed, virus levels dropped with an average half-life of 48 minutes. After the new liver was implanted, they found that virus levels continued to drop for up to 23 hours, then began to rise, doubling every 2 days.

Notably, in three patients, the virus levels plateaued before rising, suggesting, say the authors “that a non-hepatic source supplied virions and balanced their intrinsic clearance.” The authors estimate, however, that non-hepatic sources can only account for 4 percent of total viral production. Ninety-six percent of it occurs in the liver.

The patterns of viremia decline and increase seen in this study are consistent with previous studies, although this study indicates a much faster virion half-life than previously suggested. The findings also support the notion that HCV can replicate rapidly in the post-transplant immunosuppressed patient, leading the authors to suggest that early anti-HCV therapy may delay or prevent reinfection.

The study was limited by the small number of patients and the single compartment model, which did not separately account for liver and extrahepatic sites of viral replication. “Nevertheless,” report the authors, “the rapid HCV RNA decline in the anhepatic phase, followed by the postoperative increase observed in several patients…suggest that the liver is the primary site of viral replication, with at most small contributions from extrahepatic sites.”

In conclusion, the authors write, “Continued work towards elucidating extrahepatic replication, the time-course of reinfection, the effects of immunosuppressive therapy, and the relationships among viremia, infection and liver damage will be beneficial in optimizing treatment for HCV patients undergoing liver transplantation.”

02/03/06

Reference
K A Powers and others. Kinetics of Hepatitis C Virus Reinfection after Liver Transplantation. Liver Transplantation 12(2): 207-216. February 2006.