Aa
Cirrhosis of the liver
Is there anyone here who is suffering fromt this disease? If so, did you find help in rehabilitation? I will tell my own story after I know that I am in the right place.
Would love to hear more about this new treatment coming out that kills the virus in 3 days!!! Can you attach the links or give me information on when this should be available in the US for treatment? Who do I talk to about getting into a trial?? Any information would be great!
As most of you are aware, my 15 year old daughter has stage 4 and has not responded to any treatment so far.. Contracted from me at birth. Currently on daily infergen, don't think she is responding to this either...Already tried Pegasys and Peg Intron with little success. We are thinking of adding zadaxin to this or Pegasys next. I am going crazy with worry. Don't know how I am coping any more...She just dosn't get a break...I need to find something that will work...Her albumin is slipping below normal now which probably means her liver took a turn for the worse even with this past 52 weeks of treatments. Any information you could provide about new treatments and when they will be available would be great.
Thank you
Jodi
As most of you are aware, my 15 year old daughter has stage 4 and has not responded to any treatment so far.. Contracted from me at birth. Currently on daily infergen, don't think she is responding to this either...Already tried Pegasys and Peg Intron with little success. We are thinking of adding zadaxin to this or Pegasys next. I am going crazy with worry. Don't know how I am coping any more...She just dosn't get a break...I need to find something that will work...Her albumin is slipping below normal now which probably means her liver took a turn for the worse even with this past 52 weeks of treatments. Any information you could provide about new treatments and when they will be available would be great.
Thank you
Jodi
Some of the newer folks here seem to be taking aspirin during tx. Many studies have shown aspirin to negatively affect platelet production. Not a good idea along with interferon and riba which do their own number on platelets. Stick with Tyelenol of ibuprofen as directed by your doctor, folks.
Hi, Magnum,
When you read about these studies, did they involve just a few days of protease inhibitors, or did the patients then continue with a course of interferon based therapy?
Some of the early trials (B.I. last year) showed promise in super rapidly knocking the viral load way down (we have no test that measures down to VL=0, as far as I know); those patients were not taking interferon tx; when the Protease Inhibitors were stopped, folks got their starting viral load back in about a week.
If you have any virus left, unopposed, it will double every couple of hours. That is why relapses happen so fast after tx is stopped and the drugs drop below therapeutic levels. Within a week, you can be back at whatever VL your body could handle.
So if you know of anything coming down the pike that doesn't involve (pegylated) interferon based tx, please post about it. From where I'm reading, it looks like everything for the foreseeable future will involve interferon, and probably ribavirin. If we're lucky, Protease Inhibitors, etc. will shorten the duration of tx and improve the SVR-odds for all genotypes.
Maj Neni
When you read about these studies, did they involve just a few days of protease inhibitors, or did the patients then continue with a course of interferon based therapy?
Some of the early trials (B.I. last year) showed promise in super rapidly knocking the viral load way down (we have no test that measures down to VL=0, as far as I know); those patients were not taking interferon tx; when the Protease Inhibitors were stopped, folks got their starting viral load back in about a week.
If you have any virus left, unopposed, it will double every couple of hours. That is why relapses happen so fast after tx is stopped and the drugs drop below therapeutic levels. Within a week, you can be back at whatever VL your body could handle.
So if you know of anything coming down the pike that doesn't involve (pegylated) interferon based tx, please post about it. From where I'm reading, it looks like everything for the foreseeable future will involve interferon, and probably ribavirin. If we're lucky, Protease Inhibitors, etc. will shorten the duration of tx and improve the SVR-odds for all genotypes.
Maj Neni
Protease inhibitors disrupt hepatitis C replication
BY LAURA BEIL
The Dallas Morning News
DALLAS - (KRT) - Texas scientists have discovered how the hepatitis C virus can disarm the body's defenses, allowing it to become a permanent occupant inside cells.
Laboratory experiments published online Thursday in the journal ScienceExpress also suggested that drugs already being tested in patients could restore the crippled immune response, allowing a cell to rid itself of virus within days.
The discovery offers a blueprint for new treatments of the deadly infection.
Hepatitis C, which is most commonly spread through contaminated blood or IV drug use, often leads to a persistent, chronic infection. It is the leading cause of liver transplants in the United States. Under the best circumstances, current drugs - which must be taken for months, and come with sometimes brutal side effects - only cure about half the people who try them. An estimated 3.9 million Americans have been infected.
"There's a desperate need for new, more effective drugs to fight hepatitis C," said Michael Gale, a researcher with the University of Texas Southwestern Medical Center at Dallas. Gale and colleagues from the University of Texas Medical Branch at Galveston conducted the new experiments.
The research team discovered that the hepatitis C virus drops a kind of precision bomb once it invades a cell, releasing an enzyme that disables a molecule called interferon regulatory factor 3, or IRF-3. Without IRF-3, the cell's immune response stalls. With the immune system no longer around to restrain it, hepatitis C gains free reign of the cell, making copies of itself, and moving on to infect other cells.
But the UT Southwestern scientists were able to restore IRF-3 by exposing the cells to drugs called protease inhibitors. Once the cell was awash in protease inhibitors, the hepatitis C virus was unable to take over. The cell's immune system resurrected, and the virus vanished.
"This is, I think, the weak link in the virus's ability to persist," Gale said.
And pharmaceutical companies are already testing protease inhibitors in small groups of patients, Gale said, so experts should know soon how the drugs fare in patients, not just cells.
A second paper published with Gale's study explains more about how IRF-3 and its team of molecules protect cells. "This is a mechanism that is actually used by many viruses," said John Hiscott of McGill University in Montreal. The fact that protease inhibitors restored IRF-3, he said, has implications for many viral infections beyond hepatitis C.
Hepatitis C experts, meanwhile, are pleased to have a new avenue to pursue. "We found something else that may give us a handle on getting rid of this virus," said Leslye Johnson, who heads research into liver infections at the National Institute of Allergy and Infectious Diseases. If Gale's discovery leads to a better, easier treatment for hepatitis C, she said, "It will be a blessing for the population."
Other UT Southwestern researchers involved in the study were Eileen Foy, Chunfu Wang and Rhea Sumpter.
---
BY LAURA BEIL
The Dallas Morning News
DALLAS - (KRT) - Texas scientists have discovered how the hepatitis C virus can disarm the body's defenses, allowing it to become a permanent occupant inside cells.
Laboratory experiments published online Thursday in the journal ScienceExpress also suggested that drugs already being tested in patients could restore the crippled immune response, allowing a cell to rid itself of virus within days.
The discovery offers a blueprint for new treatments of the deadly infection.
Hepatitis C, which is most commonly spread through contaminated blood or IV drug use, often leads to a persistent, chronic infection. It is the leading cause of liver transplants in the United States. Under the best circumstances, current drugs - which must be taken for months, and come with sometimes brutal side effects - only cure about half the people who try them. An estimated 3.9 million Americans have been infected.
"There's a desperate need for new, more effective drugs to fight hepatitis C," said Michael Gale, a researcher with the University of Texas Southwestern Medical Center at Dallas. Gale and colleagues from the University of Texas Medical Branch at Galveston conducted the new experiments.
The research team discovered that the hepatitis C virus drops a kind of precision bomb once it invades a cell, releasing an enzyme that disables a molecule called interferon regulatory factor 3, or IRF-3. Without IRF-3, the cell's immune response stalls. With the immune system no longer around to restrain it, hepatitis C gains free reign of the cell, making copies of itself, and moving on to infect other cells.
But the UT Southwestern scientists were able to restore IRF-3 by exposing the cells to drugs called protease inhibitors. Once the cell was awash in protease inhibitors, the hepatitis C virus was unable to take over. The cell's immune system resurrected, and the virus vanished.
"This is, I think, the weak link in the virus's ability to persist," Gale said.
And pharmaceutical companies are already testing protease inhibitors in small groups of patients, Gale said, so experts should know soon how the drugs fare in patients, not just cells.
A second paper published with Gale's study explains more about how IRF-3 and its team of molecules protect cells. "This is a mechanism that is actually used by many viruses," said John Hiscott of McGill University in Montreal. The fact that protease inhibitors restored IRF-3, he said, has implications for many viral infections beyond hepatitis C.
Hepatitis C experts, meanwhile, are pleased to have a new avenue to pursue. "We found something else that may give us a handle on getting rid of this virus," said Leslye Johnson, who heads research into liver infections at the National Institute of Allergy and Infectious Diseases. If Gale's discovery leads to a better, easier treatment for hepatitis C, she said, "It will be a blessing for the population."
Other UT Southwestern researchers involved in the study were Eileen Foy, Chunfu Wang and Rhea Sumpter.
---
Thanks, Magnum.
I know that several major studies are going on with the protease inhibitors, and there is keen competition to be first on the market. It is reminiscent of the PegIntron/Pegasys introductions; I'm grateful we have both those meds now. Dr.Gale/UT leads one major group, and B.I.in Germany represents another on the leading edge w/protease inhibitor studies.
They can't guarantee a VL=0 from the studies yet, as there are no tests to determine VL=0. I guess the Quantasure (have I got this right, Galen?) and Quest's Heptimax are the most sensitive PCR's out there, going down to 2 and 5 I.U./mL of blood, but they don't go to absolute zero. Thus there is a chance that a few very hardy "Super Darwinian Kings of Evolution*" viruses might survive and start replicating after the drugs are stopped.
(*I don't remember who introduced that phrase here... but thanks)
That's why the 6 mo. post tx test is the diploma for SVR, because relapse usually happens within a month or two.
The way I see it, an interferon combo tx will still be used to mop up, perhaps of shorter duration and with smaller dosages. This is one reason why there need to be further studies to refine dosing, duration, and criteria/tests for the new protocols to come. May they come soon.
Maj Neni
I know that several major studies are going on with the protease inhibitors, and there is keen competition to be first on the market. It is reminiscent of the PegIntron/Pegasys introductions; I'm grateful we have both those meds now. Dr.Gale/UT leads one major group, and B.I.in Germany represents another on the leading edge w/protease inhibitor studies.
They can't guarantee a VL=0 from the studies yet, as there are no tests to determine VL=0. I guess the Quantasure (have I got this right, Galen?) and Quest's Heptimax are the most sensitive PCR's out there, going down to 2 and 5 I.U./mL of blood, but they don't go to absolute zero. Thus there is a chance that a few very hardy "Super Darwinian Kings of Evolution*" viruses might survive and start replicating after the drugs are stopped.
(*I don't remember who introduced that phrase here... but thanks)
That's why the 6 mo. post tx test is the diploma for SVR, because relapse usually happens within a month or two.
The way I see it, an interferon combo tx will still be used to mop up, perhaps of shorter duration and with smaller dosages. This is one reason why there need to be further studies to refine dosing, duration, and criteria/tests for the new protocols to come. May they come soon.
Maj Neni
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