Why does the virus come back with vengeance after

a relapse occurs in most patients and what could be done differently to change the out come?

[Myown]

I've heard that the virus usually comes back with a vengence, but for some reason mine was "only ?" 87,000 at around 8 or 9 weeks post. My baseline VL was over 8 million so I was surprised when I relapsed that it wasn't around 8 mill when tested. But now it has climbed back up and the last test it was 7 million - that was about 5 months post or so - now I am 6 months post and I'm curious as to what it is at this point.

[Myown]

I wondered if maybe mine wasn't real high and thought that maybe my body was trying hard to fight it. I don't know I am only guessing, but since the body DOES try to fight it, this was my first thought when the doctor first read the lab to me - the dreaded day - yuk.

[geterdone]

WOW! it took 20+ years for most to get to that viral load and then 48/72 weeks to knock it down or to get to UND, Ok, and so it only takes 6 months to re-replicate back into the high numbers??? I don't understand why this happeneds.

jasper

[Myown]

I am 2b so I only tx 24 weeks not the 48 - next time 48 though. But ya know what I have read that for alot of people the high numbers come back immediately if they relapse.

I was UND at 4 weeks post tx and being I was RVR my particular situation is kind of hard to understand. My doctor thinks that its just a matter of txing longer. IMO its a real cr@p shoot when a geno 2 has a high VL cause 24 weeks just might not do the trick - though it has for some even at 16 weeks. I would have rather have gone to 48 weeks (hindsight is 20 -20)...and now that I have to tx for 48, I would actually like to go longer if it were possible with insurance and if I don't have difficulty with sx.

Happy New Year. And I hope to hear great news of your SVR this year.

[geterdone]

Happy New Year to you too.  

“MY doctor Thinks”, this in it self is the scariest part of all… I have thought a lot in the last 43 weeks and have learned a lot more about what this virus has in tailed for me and am in just as much a flux as treating doctors which leads me to the next thought.

While dropping back and regrouping from the disappointment of relapse what do we turn our minds to? Is there a should of, could of, and if I had only done things differently, what would you have changed as far as your treatment, diet and life style? With what you know about HCV at this point and/or have learned over the past weeks, years here on this board about the treatment process and monitoring stages during the course of treatment, what would you try to change in that process or bring up in a conversation with your old/new doctor before retreatment?
Would you go into a consultation armed with the knowledge learned and debate your points and back them up with data and research to get the doctor to take you more seriously about your treatment and recovery?
It seems quit obvious that most doctors (GI), and specialist are following a standard play book (inside the box), so to speak; as far as SOC treatment and are less likely to listen to a patient who has done research on their illness and in most cases have more up to date information available to them to aid in there own recovery but as with most doctors will not listen to what their patients have to say even tho the patients are the ones who have to endure the treatment with a 50/50 chance of SVR at the end of 24/48/72 weeks or longer of treatment.

[jmjm530]

To simplify -- and there will be some speculation in this post -- the virons replicate quite rapidly, but they are also killed quite rapidly by the immune system.

The viral load numbers you are left with on testing, represent let's call it "last virions standing" from this continuous battle. And while viral load itself does not correlate with liver damage, studies do suggest that lower viral loads are easier to treat.

Is this because there are less virons to kill, or perhaps because fewer virions indicate that the immune system is stronger at that particular point in time and therefore will be more likely to succeed once the interferon is added?

If you buy into the latter scenario, then it's reasonable to speculate that someone with a lower viral load is showing a stronger natural immune response than someone with a higher viral load.

And because viral load can significantly fluctuate over time, it seems reasonable to explore  coordinating the start of treatment with a viral load "trough", i.e. when VL is very low.  Of course this has a number of logistical issues including frequent VL tests and the fact that some may need to treat right away as opposed to waiting, not to mention that some people may never have their viral load go into the low zone.

This also brings up the issue of exploring ways to reduce viral load prior to treatment, but to my kmowledge no reliable path has been demonstrated to date. For example, several devices report lowering viral load by treating the blood with some sort of light source, but no follow-ups I know of either to colloborate the findings or to show how this technique might translate into higher SVR rates. It could in theory, but on the other hand, if it doesn't affect the immune system, it might not.

MO,

In your case, what your low post tx viral load may have meant is simply that your immune system was doing a pretty good job of killing or supressing (pick one depending on your orientation) the virus -- just not good enough job. So, if you decide to re-treat, your doctors advice to treat longer with the same drugs seems reasonable.

Curious, what weeks did you test for viral load during treatment, and what was the sensitivity of those tests? If I remember correctly, you might have missed the week 4 test? It's also becoming apparent, that testing periodically after UND using sensiive assays is also becoming increasingly important to predict SVR.

-- Jim

[Myown]

Curious, what weeks did you test for viral load during treatment, and what was the sensitivity of those tests? If I remember correctly, you might have missed the week 4 test? It's also becoming apparent, that testing periodically after UND using sensiive assays is also becoming increasingly important to predict SVR.
-------------------------------------------------------------------------------------------------
JIm, I missed only the first week VL. My VL went from over 8 million to 4 hundred something by the second week. The 3rd week it was 96iu and 4th week UND. Heptimax was used. <5.
4 weeks post UND <10.

I continued to get tested every month using Heptimax until somewhere towards the end when my insurance dropped Quest. At that point Lab Corp was used <10.

The immune system is beyond hard for me to understand and I say that because I know my health has been very good and my diet etc. I considered that possibly a strong immune system might not always be the greatest thing to have when first infected - maybe the immune response is too strong??? I don't know what I am talking about and I do not know enough or hardly anything about the immune system and how it works, but can only say what I feel or discern <?  But the reason I say that maybe a healthy person with a strong immune system may work against them is because I read on forum once ,,,a poster passing thru said she is/was an addict and stuck the needle in her arm even knowing her b/f had hep c.  She went on to spontaneously clear. That struck me odd cause you would figure a person who is an addict is not in the best of health. Happy for her, but also confuses me to the max how the immune system works. So that is what led me to believe that possibly a healthy persons 'strong immune response' might be too much - stir things up and makes the virus go into a frenzy whereas someone else who is not as healthy has less of an immune response and so the T cells (or whatever cells) gently knocks them (virons) off and that person spontaenously clears. As I said, I am only going by what I feel and nothing is based on what I know about the immune system -cause I don't know anything.

Geterdone...you have some great questions. Let me get back to you. I have to run.

Ps, Jim lately I have been wondering if maybe the pegintron would be better for me. I am concerned that since my VL is or has been always so high that maybe I do have alot of virons stuck in the nooks and crannies where only a smaller molecule could reach. Plus the BBB and pegintron. But of course I do concern myself with I know I did RVR with pegasys and I wonder if it would have been the same with Pegintron. I really wish I could alternate the 2 interferons each week. They do all these studies and I bet there has never been a study with using the 2 interferons and alternating weeks. The drug companies would make the same or maybe even more money I would think and maybe there would be more people who SVR.

Seeya later.

[mremeet]

"Why does the virus come back with vengeance after a relapse occurs in most patients and what could be done differently to change the out come?"

I think most relapses occurring after treatment where a VL goes well above starting baseline value are probably associated with the abrupt cessation of interferon. The body produces its own interferon and apparently the natural production and regulation of IFN is greatly curtailed while the synthetic IFN is being introduced (especially over the course of months and months of SOC treatment). Usually once treatment ends, the synthetic IFN is simply halted abruptly. This leaves the body immunologically flat for a while, at least until it can restart and upregulate its own IFN production again. During this timeframe, if there are viable virions still remaining (as occurs in all relapsers), those virions will usually multiply very rapidly as the world they live in has suddenly become hospitable again. Not only is it hospitable, but it may even be more hospitable than it had previously been before treatment when the body's own production of interferon was at substantial levels serving to keep the virus in check. The only caveat here is that the virus' ability to bounce back with a vengeance after tx is halted is also dependent on how healthy the virus itself is. In other words, it takes two to tango when it comes to VL, and those two are the virulence of the virus and the effectiveness of the body's immune response to that virus. If the virus has been mutated into a relatively "unfit" state during its extended battle with IFN and ribavirin, this also may make it difficult for the virus to make a stunning comeback. I suspect this viral “crippling effect” likely accounts for those who do not have VL's that soar well above baseline levels after tx is ended. And incidentally, HR discussed the theory behind tapering IFN dose down after the tx cycle has concluded in a recent thread (for possibly thwarting a viral comeback until the body’s own defenses return to full capacity). This theory also ties into the idea of how the body needs time to re-initiate its own IFN production.

Another interesting thing to look at is the typical viral response of patients who undergo anti-HCV protease inhibitor monotherapy (i.e. without the help of IFN and ribavirin etc). Typically when a PI (like Telaprevir or BILN2061 etc) is introduced the VL initially drops dramatically. Then, usually within just a few weeks it rebounds right back to pre-tx baseline values. But I've never seen data that shows VL rebounding well above baseline values after concluding a course of PI monotherapy, as is often the case after a failed IFN based tx. The reason for this is probably because PI's are direct acting anti-virals, they do not depend on the immunostimulative actions of interferon or ribavirin. They work independently of these functions and in the simplest sense directly obstruct the virus' ability to replicate. Therefore, PI's do not significantly affect the body's natural production of interferon, so the body's normal IFN based immuno-response is not altered or tinkered with as occurs when synthetic interferon is introduced (and perhaps ribavirin too). The only effect I could see a PI having might be a subtle/temporary/indirect lessening of the body's immune response as a consequence of the temporarily decreasing VL (assuming "average" immune response is linked to average VL, which it probably is under most circumstances).

[wyntre9]

That's interesting.

So you think that tapering off peg at the end of TX is a good option?

wyn

[mremeet]

In consideration of the fact that tapering IFN down for a few more weeks is not harmful (within the context of the extent that SOC is harmful), and in consideration of the possible theoretical merits of allowing the body's immune responses to be brought up to speed prior to "flying solo" once again - then yes I would taper my IFN dose off at end of tx. In fact I wanted to do that at the end of my 41 weeks of tx, but this was not allowed in the VX950 trial I was enrolled in. Also, by the time I quit I was so tapped out physically that I just couldn't take any of it any more. But if I had to undergo another course of conventional SOC, then I would taper my IFN after EOT. My $0.02 anyway, don't spend it all in one place. ;-)

[wyntre9]

'My $0.02 anyway, don't spend it all in one place. ;-)'

No.  I appreciate your perspective.  I'm in the information-gathering stage, preparing for end of 72 week tx (4 months from now) and I'd like to know of any and all options availble to give myself the best chance at SVR.

I simply hadn't heard much about the tapering off.   Over the past 56 weeks I have noticed several threads regarding the issue but at the time i was so involved in whatever stage of TX I was currently wading through and the end seemed so far away that I didn't read those posts thoproughly.

Do you know of any particular studies about tapering off meds?  I'm gonna google it but you know how much garbage is out there and how time consuming it is to sift through it so any leads would be appreciated.

Thanks ,

wyn

[jmjm530]

Well, certainly no virons under the limits of less sensitive testing. I know it must be frustrating, especially because of your RVR, and that frustration no doubt continues to wear as you consider future treatment options. In a sense it would be easier if you didn't respond so rapidly and then at least you could blame it on that.

That said, unlike genotype 1's, I believe the vast majority of genotype 2's do RVR -- so maybe it's importance is more in terms of a negative predictor (i.e. if no RVR, then treat longer) as opposed to a positive predictor. Don't know what to say about the Peg Intron, and it's anyones guess if it could make a difference. As to mixing, it's an interesting idea, but why be a guinea pig given your stats?

Of course you can run all this stuff by your doctor who is very knowledgeable, however no matter how much knowledge a given doctor may have -- they still haven't pinned down how this virus really works. They're still debating, for example, what is the role of ribavirin.

In part, because of these uncertainties, I thought waiting for a PI might make sense in your case in the event that for some reason interferon and you just don't make a good partnership, no matter how long you treat. I don't think that is the case but again so much is uncertain and it's really how you want to gamble.

However, I do understand that the PI alternative is not available right now for your genotype, however it does seem to work in vitro -- and hopefully will be shown to work in real patients soon, as discussed in another thread.

-- Jim

[mremeet]

Here's a few links regarding the IFN tapering, including a google search result. Kalio did 72 weeks of tx (if memory serves) and tapered her IFN off at the end. She's SVR now, not proof that it works but certainly not "anti-proof" that it doesn't work. I don't know any controlled studies offhand that involved tapering doses of IFN after what would normally be EOT. Right now there's only theory to rely on, although IMO the theory makes enough sense to implement into action.

http://www.medhelp.org/posts/show/370191

http://www.medhelp.org/forums/hepatitis/messages/46125.html

http://www.google.com/search?q=HR+IFN+tapering+site:medhelp.org&hl=en&rlz=1T4GWYF_en___US236&start=0&sa=N

[wyntre9]

Thanks for the links.

I'm gonna check them later.  

Happy New year.  :)

wyn

[geterdone]

Thanks for the links and recognized the one but did not see message 46125 back then because Hal had the controls, lol and was unaware that hr and others discussed this very out of the box end of tx approach before.

I am having problems copying and pasting the link into google search, do I copy the whole link or just part of it?

Thanks!
Jasper

[wyntre9]

46125 just popped up when i pasted into the browser bar.  Same for the google link.

wyn

[geterdone]

I'm sorry I should have been more clearer; I was trying to past the third link provided by mr into the google search but it brings up nothing.

jasper

[wyntre9]

That's what I was trying to tell you;  just copy and paste the whole thing into your browser bar and what pops up is all medhelp threads on the topic.  At least, that's what happened for me.

But when i pasted to Google Search I get an error message.

i tried to copy the page to show you the contents (there are 3 pages) but can't do that.  

wyn

[geterdone]

HA! lmao, duh?

Thanks
jasper

[wyntre9]

Mrmeet did some trick the CI's (computer-impaired) amongst us aren't aware of.

Wish someone would explain, in very simple language, how to DO that.

:)

wyn

[geterdone]

Yeah, at times it seems that way but keeps me spinning, lol!
mremeet, thanks for the links, they cover most of my question and also fills some holes.

Thanks
Jasper

[merryBe]

MrM thanks for the good explaination info....I do have enough INF to taper off and intend to, it's way too logical not to.

Jasper, what to do different?
I've only known for 6 months I've had this, but I think monitoring IGF-1 level, insulin, fat consumption, and all the things Jim and HR are always mentioning probotic/pre....antifibrosis wise etc. could all be critical factors.

Well, mentioning this idea that I was going to eliminate the excess weight now that my pituitary was working again....this was the only spark I got out of my "team" ... when I said I was down 40 lbs and intended to get the other 40 off as well. Evidently, going on HGH has now allowed my metabolism to approach normal levels, meaning I can once again burn calories whereas before I barely did.
Now carrying extra weight is important for lots of reasons, and many HCV patients do NOT have normal functioning pituitary...which means they are in a catch 22 when it comes to immune response as well as normal metabolism.

the reason I think maybe this approach may have validity is based on the stats of who clears, the young and the lean do a far better job. Maybe, it's like any other virus, while your body fights a bug, your system doesn't need a lot of other things to deal with, like either digesting too much or carry around and nourishing too many stored calories.
It may be also that the virus itself is what causes the pituitary function to slow way down, they don't know yet.
In any case, there's also the question of where and how do virus's hide.  A while back I asked, does anyone think maybe this one hides in fat?  Like we know the chicken pox virus and herpes hide in spinal fluid...but not every virus hides in the same place. So just like critters, some get under rocks, in trees, you name it..it could be that the lower caloric intake is what's giving the lean the better success rates, or, it could be the fat itself, which produces it's own set of chemicals like estrogen, etc etc may make the whole system more virus friendly.

In any case, I'm sorry to hear you are having to go through this also...it suucks.
Time to just regroup and consider how many ways can we find to improve not just our odds, but our quality of life going forward. L'm not sure I would give up one holiday meal a year....oh perish that thought, but it's important to give our bodies a fighting chance.
I wouldn't kick yourself if you had one piece of halloween candy for instance, but giving up even the occasional libation or the "weekly" treat could just make the difference.
I know they made a huge deal out of the alcohol/pot consumption both at the clinic class, and in here...but I'm starting to think that the case HR and others make for calorie consumption/not overloading the liver ever, etc may play as big of a part. Who knows.

In any case, I wouldn't kick yourself around about it, for all we know if every relaspser had done everything perfect this little colony still would have reseeded itself.
there does seem to be some correlation however between diebetes (diabetes) and relapse, which makes me think the virus may thrive more in a calorie rich blood supply.
If you'll notice when the body gets a virus, it naturally restricts it's own calories...just food for thought.

[jmjm530]

Losing that additional 40lbs and getting down to an ideal BMI could be the single most important thing you can do to give you a bettter chance the next time you treat. The other pre-tx "prep" would be to reduce iron load -- perhaps through phlebotomy -- prior to treatment, assuming of course it needs to be reduced.

-- Jim

[jmjm530]

Forgot to mention cigarette smoking if relevant. I believe I read a study where it can impact negatively on SVR.

[BThompson4]

I did 72 weeks and had <25 iu/ml pcrs every two weeks from time of being undetectable at week 22.  They were all undetectable except week 53 which showed 43 iu/ml, which hep docs said was probably a false positive.  Four weeks after tx viral load was 3.7 iu/ml, so it obviously came back very strongly and quickly after tx.  Who knows when better tx will become available.  HR says 2011, which is farther down the road than most here have speculated.  I am immune suppressed, and my new liver took only 3.5 years to get to F2 fibrosis after transplant, and the F2 biopsy was done in June 2005, a full year before starting tx, so it was probably even more damaged when I started tx.  I had biopsies in March (F0-F1 damage found) and November (F1 damage found) of 2007 which showed pretty dramatic fibrosis improvement, assuming that I was F2+ fibrosis prior to tx, which I probably was.  Disappointed about not staying UND, but very glad I did the tx, even the whole 72.  Hep C damage post-transplant can be very rapid, and I probably bought some time to eventually get the new drugs.  I am six weeks post-tx and already feel better than pre-tx, so I have no regrets that might come from having long-term post-tx symptoms.   Who knows how much and how quickly damage is done by the virus post-tx though.

[cruelworld]

i hope you havent really relapsed. i dont understand 3.7 iu/ml viral load, i know of no test to even get this number.  based on your statement about coming back strongly i assume you mean 3.7 log iu/ml. still not a big number but i guess enough to signify
a true relapse. i hope that this turns out like nygirl and you end up with an svr.

[BThompson4]

Sorry about the 3.7.  I left out the million.  It is actually 3,760,000 iu/ml, or 6.58 log iu/ml.  I wish it had been that low!

[cruelworld]

what a heartbreaker. all that testing , misery and overdosing,
at least its over for a while and you can live again.
i know progression is faster for tp's but it seems like you should have a decent time margin for new drug opportunities. by now you are certainly a venerated warlord
and i have every confidence you will see this through to final victory.

[geterdone]

"Fat consumption", (lipids) cholesterol and lipid rafts. Cholesterol is more abundant in tissues which either synthesize more or have more abundant densely-packed membranes, for example, the liver. Caveolae are one source of clathrin-independent endocytosis involved in turnover of adhesive complexes.

Sometime I wonder if the intake of Fats with the riba may be working against the fight to entirely eliminate the virus and in fact may be aiding in its hiding ability either in whole or in part due to the dismantling of the virus chain through treatment but not eliminate the segmented parts which flow through the blood stream attached to or imbedded in the cholesterol with the encoded dna (the glove) which has built up a resistance to the riba, inf and our own immune system and when the virus population is all but eliminated through treatment, UND status and at the eot when our immune systems are trying to readjust these segmented parts missed by std. pcr’s because of the buoyancy of the cholesterol has allowed them to escape such present test, begin to flow freely with in the blood once more and reconnect to the other segmented parts thus re starting the virus chain again in which relapse may or may not be imminent.

Probably not be correct but points to ponder…

jasper

[Myown]

Well, certainly no virons under the limits of less sensitive testing. I know it must be frustrating, especially because of your RVR, and that frustration no doubt continues to wear as you consider future treatment options. In a sense it would be easier if you didn't respond so rapidly and then at least you could blame it on that.
------------------------------------------------------------------------------
Yes its frustrating because the trolley train that I always talk about is the Medical worlds answer. If I didn't use weight based or something like that, then I would be going into tx with a positive attitude such as "well now it will work cause we are going to up the riba." But the riba was weight based so i can't use that to say this time it will be all good,

There are several things that still were not done properly(recently too) and even someone like me who has lots of hutzpah to push for things to be done correctly - I am worn out and my husband says if he wasn't there or it it was someone else telling the story, he would have a problem believing how some of these things were handled and continue to be handled the same way.

I just have to continue to push and shake the tree and let my voice be heard and let them know that their method of putting people back on the "trolley track" and only change being the trip is longer - does not or might not work. Proof of the pudding is they have put some back on the trolley 6 or 7 times and never even looked to see if there was something they could change AND IF change did occur in the mix, its usually ONLY because the patient was very vocal it seems.

This virus is alot of work for the doctor and patient and that's if you just follow normal procedure. When you start to ask a doctor questions like - look at my hormones how off they are - how do you think this is affecting my tx,,,my dhea is 3 x's higher than what it is supposed to be - Dhea is the foundational hormone, how is this maybe affecting my tx?? Have other relapsers had high DHEA such as this??? Well those answers can never be answered cause when you fail tx,,,again,,,all you hear is a whistle blowing and someone yelling "All Aboard....."

I don't plan on doing tx over and over and over with doctors that tell people oh okay we did 24, then 48,,,,"ohhhh, I know, lets do 72 now,,,,you're sure to win with 72:)

Nope they have to call in other doctors with this disease. Its great to have a "liver specialist" cause the disease is a "liver disease", right? NOT....We all know its not,,,,AND HEPATOLOGISTS yes are better than the GI, but we still need " added minds -(specialists)" at least for the more difficult cases to start.

So thats the story.  I am excited to start. I look forward to getting rid of the virus, but just as I didn't feel all the loose ends were tied before I started last time, I still have that feeling. I proved myself right last time by not svr and this time I don't want to be right so these doctors are going to have to work a little harder and look a little closer before I start this time. Let them all call me a PITA, I don't care at this point. I've been easy. My NP has her nose up in the air cause I don't use her anymore, but I am not there to help her career blossom, I am there to get well. And its evident that my doctor likes the one on one with patients. I know some think, "oh these big doctors need to be doing more research, don't be selfish and insist on seeing the doctor."  Well thats a stupid.....that would be like telling a musician not to do anymore rock concerts so that you will have more time to write songs..... a musician needs to sing and some doctors need that "one on one," cause they truly love dealing with patients. I believe thats the case with my doctor cause he is ALWAYS in a good mood and its easy to see he loves what he is doing.

So I'll see what the latest is the next time I go. He wasn't interested in using Alinia. I'll ask him if I could use 2 different interferons or maybe I should switch to pegintron. He is more for Pegasys probably:) So I don't know how much he uses the other AND IF he thought the other was more suitable I would want it. Its funny cause the other consult I had I told my husband this doctor will say Pegintron cause I know thats his fav from what I have seen him use in studies and sure enough that is what he suggested, but at that time I wasn't sure and felt safer with pegasys cause no sx etc. he agreed to it after I said that. So if I deceide to go toPegintron I know I would have no problem getting it at that office if I tx there. I will be looking at a few things as to decide where to tx. Lots of deceisions again.

See ya later.

[mikesimon]

I'm sorry to learn about your relapse. When I relapsed I saw the same type of VL. Mine 2.5 weeks after stopping was 6.85 million and the highest it had been previously was 2.8 million. But, 5 or 6 weeks later when I began re-treatment it was 3.4 million. Probably not a significant drop but it looked better to me. When I went from <5 IU/ml to 6.85 million in less than 3 weeks it was shocking, to say the least.
I wish you the very best this new year.
Mike

[Proactive]

I as well am sorry to hear about your relapse, and after enduring 72 weeks of tx to....damn!
I am trying to prepare myself for any bad news which might arrive down the road, but I guess unless you've been there and done that, it's difficult to fully comprehend. agian, sorry...
Bill mentioned the other day, as he's in week 68 or so, he was getting antsy/nervous about finishing tx and stopping the meds...I can relate in full, with 10 weeks left I am already getting worried about stopping the meds....They almost become our crutch over time, as long as we are on the meds we kinda have a safety net.....Best of luck this upcoming year, and keep us posted on your decision making process........Pro

[Myown]

While dropping back and regrouping from the disappointment of relapse what do we turn our minds to? Is there a should of, could of, and if I had only done things differently, what would you have changed as far as your treatment, diet and life style? With what you know about HCV at this point and/or have learned over the past weeks, years here on this board about the treatment process and monitoring stages during the course of treatment, what would you try to change in that process or bring up in a conversation with your old/new doctor before retreatment?
---------------------------------------------------------------------------------------------------------------------------------------------
Well, ya know what it really depends on you it is that has the relapse. I am a "woulda,shoulda, coulda" person from the time I came out of my mothers womb. So I am not a 'relapser" that should be interviewed cause I am not a middle of the road person where you can get a 'good perspective' on things. I'm usually extreme in one way or the other and thats not always good. Some times and for some reasons it could have its benefit in being extreme, but I don't think its good to be this way when you have a disease.

One thing I would have done differently- a bx prior to tx. I didn't have one until after relapse. I would now tell people that bx yes are the gold standard as I was told, but besides showing grade stage, other things may show up. In my case microgranulomas showed up. I would have liked to have known if I had these prior to tx or they appeared after tx. We will never know at this point.

When I came to forum I read so many posts of people losing 20 pounds and even more and some who may be pulled from tx if weight continued to drop. That made me nervous cause I thought I would be sick all the time and hardly eating and get too thin, so I purposely added weight on so that if I lost weight I had some extra to start with. I didn't get sick and so the extra pounds didn't need to be there. So thats another thing I will do different this go round. I need to drop a few more to be my my exact weight of what I should be.

Any of the doctors that I will be txing with are involved in all the latest studies so as far as bringing studies that won't help, cause they know them all. So as far as telling the doctor the 'latest' things out there, they are aware, but thats not always a plus either cause a doctor that isn't aware really hasn't formed an opinion and it might be easier to get a doctor to add Alinia who has never heard of it, than someone who is "up on everything." My doc said no Alinia - only done with g 4 so far. I knew that - we all know that from forum,,,but I wonder if I was going to just the average GI doc if he would have said "oh that sounds exciting, lets give it a try."  (So I think you can see that my conversation thus far exemplifies a 'woulda coulda shoulda kind of woman.:)

Another thing that I think I will change is........
I think I spent waaaaaaaaaay too much time on forum last tx.So this time that will change and I'll just be in contact with those who email or call me and come to forum when I have a question.

I thank God for this forum and all the great people who have helped me so much, but I think I held on to the forum too tight and my world was and is all about Hep c and nothing else. I feel I lost myself somewhere. Meds cause personality changes and I'm now coming back to where I feel I am more myself, but thats to change soon again with tx coming up somewhere around the corner.

This time I will probably need procrit or something due to longer tx time and  I will need to come to forum for questions answered about that cause it seems the forum members explain the use of procrit better than the doctors cause it seems everyone is confused about how to use it when they first start. So other than coming to forum for questions like that, I think I am going to try to avoid forum for 48 weeks so that I don't get addicted to forum again and lose 48 weeks out of my life.

I found something that I have really been looking for for yeaaaaaars. An awesome piano player/teacher with online courses that are incredible to train your ear and I need more help in that area and my mouth dropped when I found this guy. He's awesome and he goes into some very advanced teaching and thats what I need. So at the end of 48 weeks I hope my piano skills will catch up to my vocal skill. If I fill my mind with something I love (music) I think that will have a positive affect on my tx.


So Jasper as I go round and round, what I am trying to say is I want to fill my life with things that I used to have in it prior to dx. I have been a deer stuck in the headlights from the moment I heard "you have hepatitus (hepatitis) C." So that is something I want to change this next go round. Less time on forum, so that my mind somehow gets a break from hep c - if thats possible.

I probably did a very poor job on answering your question and I am really just emptying what is in my mind at this moment and not looking at the whole picture. I'm sure there are other things that I will change but right now this is all I can come up with.

I hope you are feeling good these days and that everything works out for you.
MO

[gauf]

Therefore, PI's do not significantly affect the body's natural production of interferon, so the body's normal IFN based immuno-response is not altered or tinkered with as occurs when synthetic interferon is introduced (and perhaps ribavirin too). The only effect I could see a PI having might be a subtle/temporary/indirect lessening of the body's immune response as a consequence of the temporarily decreasing VL (assuming "average" immune response is linked to average VL, which it probably is under most circumstances).
-------------------------------------------------------------------------------------------------------------
Wondering how subtle a lessening of the body's immune system response may be. If an antiviral does not effect the bodys' own ramp up rate of natural interferon, perhaps increasing the antiviral (i.e. Alinia) while decreasing the peg may help to kill off the little buggers hiding out. What do you think?

[willing]

bt : sorry about the relapse. As hr points out in the curcumin thread, a strategy focused on fibrosis containment, even if somewhat "half-baked", may be a better bet than waiting for more-effective anti-virals. All the best.

all: I believe the kinetics of viral reproduction are fast enough that, unless the body learned appropriate HCV-specific B and T cell response during tx, infection-as-usual, ie the pre-tx steady-state, is re-established in fairly short order once the external ifn source is shut off. There's a plausilble argument for the benefits of  a "tapering"/training-wheels" approach  but I don't believe there's any data to support it.

Unfortunately serum VL is a very poor estimate of  actual cellular infection. What's being measured is only the ability to clear extra-cellular virions from circulation and any damping effect on viral reproduction. Changes in VL are a very useful  gauge of the body's response to  antiviral drugs (which is why they're so critical during the 1st 12 weeks)  but they don't say  much about the extent of  underlying  cellular infection.

[mremeet]

bthompson real sorry to hear of the relapse, that's gotta be tough considering how much time and effort you put into it. Did you see all the antifibrotic advice that HR gave in regards to supplements and diet? Might be a good strategy to employ while you wait for the PI's to become available. Considering you did persistently reach UND status on SOC drugs alone, I would be optimistic that you can "geterdone" with a PI and perhaps alinia thrown in for good measure when your time to treat comes again. Hang in there in the meantime, better times are ahead.

gauf within the context of a short course of PI monotherapy (the whole shootin' match is usually over within 2-4 weeks) which is always a failure, my guess is that it doesn't have any appreciable effect on the host's immune system. Certainly no side effects related to immunomodulation (either up or down) in monotherapy trial participants are mentioned. The only things that are usually reported in any meaningful amount are gastrointestinal issues and perhaps skin irritation. The only exception I can see would be if an allergy to the PI develops, as occurred with me after taking the PI for almost 8 weeks. Otherwise, what I said about the immune response possibly being slightly and temporarily curtailed was purely speculative. The only reason I posit that is because if the body senses a ragingly high VL in a chronically infected person, normally it will kick up its immunoresponse (and IFN production) in order to bring the virus back to more manageable levels (and this is how some acutely infected people can clear naturally). So using "layman's logic" I could see where the immune response might attenuate slightly if the VL suddenly dropped by 4 logs out of the clear blue sky (as a consequence of taking a PI) for no immunologically discernable reason.

[mremeet]

"Unfortunately serum VL is a very poor estimate of  actual cellular infection. What's being measured is only the ability to clear extra-cellular virions from circulation and any damping effect on viral reproduction."

To the best of my knowledge, effective antiviral therapy (that's capable of leading to SVR) does curtail cellular virion production, doesn't it?


Changes in VL are a very useful  gauge of the body's response to  antiviral drugs (which is why they're so critical during the 1st 12 weeks)  but they don't say  much about the extent of  underlying  cellular infection.

[mremeet]

"Unfortunately serum VL is a very poor estimate of  actual cellular infection. What's being measured is only the ability to clear extra-cellular virions from circulation and any damping effect on viral reproduction."

To the best of my knowledge, effective antiviral therapy (that's capable of leading to SVR) does curtail cellular virion production, doesn't it?


Changes in VL are a very useful  gauge of the body's response to  antiviral drugs (which is why they're so critical during the 1st 12 weeks)  but they don't say  much about the extent of  underlying  cellular infection.

[mremeet]

"Unfortunately serum VL is a very poor estimate of  actual cellular infection. What's being measured is only the ability to clear extra-cellular virions from circulation and any damping effect on viral reproduction."

To the best of my knowledge, effective antiviral therapy (that's capable of leading to SVR) does curtail cellular virion production, doesn't it?


Changes in VL are a very useful  gauge of the body's response to  antiviral drugs (which is why they're so critical during the 1st 12 weeks)  but they don't say  much about the extent of  underlying  cellular infection.

[mremeet]

"Unfortunately serum VL is a very poor estimate of  actual cellular infection. What's being measured is only the ability to clear extra-cellular virions from circulation and any damping effect on viral reproduction."

To the best of my knowledge, effective antiviral therapy (that's capable of leading to SVR) does curtail cellular virion production, doesn't it?


Changes in VL are a very useful  gauge of the body's response to  antiviral drugs (which is why they're so critical during the 1st 12 weeks)  but they don't say  much about the extent of  underlying  cellular infection.

[mremeet]

Oops, comp malfunction there. To finish...

To the best of my knowledge, effective antiviral therapy (that's capable of leading to SVR) does also curtail cellular virion production, doesn't it? And if this is true, then wouldn't the measured serum VL be an indicator of both circulating viral clearance and decreased hepatocyte production? I know you wouldn't be able to tell how much the production of new virions had been curtailed, but the measured serum VL would be dependent on both of those variables, no?

[willing]

yes, on the basis of only an observed VL measurement I don't see how one could distinguish those two effects. Presumably the presence of neutralizing anti-hcv antibodies and other immune mechanisms for clearing extra-cellular virus could be measured separately and then used to gauge how much of an observed  VL reduction was due to suppressed viral production within infected cells but I don't know of a study that's done this. One of the things I'd like to get around to at some point is understanding hcv cell/blood correlation a bit better...

all: btw, here's another recent data point in support of the "old virions never die, they just get clobbered into silence " occult viewpoint (with free text)

Gruener NH, Raziorrouh B, Jung MC.
Recurrence of hepatitis C virus during leucocytopenia and spontaneous clearance after recovery from cytopenia: a case report.
J Med Case Reports. 2007 Dec 4;1(1):169
PMID: 18053213

[susan400]

I wish I knew why it happened, too!  Susan

[jmjm530]

I read the abstract here: http://www.jmedicalcasereports.com/content/1/1/169

The patient was diagnosed with Acute Hepatitis C, with classical symptons of elevated enzymes, jaundice, etc. and a positive HCV RNA. Six weeks later he was UND. He was then treated with propylthiouracil and developed leucocytopenia and the virus returned at what appears to be week 28.

To me, this is a very narrow case study -- acute stage, no treatment, etc -- and does not support "old virions never die, they just get clobbered".

In fact, it doesn't even support the author's own conclusions: "his case history shows the risk of recurrence of HCV during leucocytopenia. These findings indicate that patients who are anti-HCV positive but HCV-RNA negative may be at risk of cytopenia-induced HCV reactivation."

The assumption here is that the HCV was REACTIVATED during leucocytopenia, but given the quirky and understudied nature of acute HCV and the dynamics of  spontaneous remission, etc -- it's unclear to me if indeed the HCV indeed every went away. (And you can't have reactivation if the HCV isn't first gone).

Besides again the understudied nature of acute HCV and the viral dynamics is the fact that during the acute stage of HCV, viremia may be intermittent, meaning it can move in and out of the detectible range. This alone could account for the neg following a positive.

I'm not saying that thsi occult stuff doesn't happen-- that's for another time -- just saying that this author's conclusions are not consistent with the author's own data, as often is the case with studies.

Hoping you would start off the New Year with something stronger than this in support of  the "occult". Anyway, hope you had a healthy and happy New Years and many to come.

-- Jim

[jmjm530]

Third paragraph from bottom -- meant to say "...positive following a negative..."

[willing]

Best wishes for a happy new year (and many more!). I suppose subjective assessment  of the strength of a piece of evidence is why we rely on juries.. but IMHO this is a pretty straightforward case (the whole article is open access BTW)

- the acute stage of infection *is* in fact well-studied; it just doesn't come up much around  here.. we've all gone through of it, this guy, probably thanks to a vigorous CTL response was one of the lucky 20% who cleared on his own.

-  HCV-RNA and other test results are  given at the close of the paper (see their Table 1). The readings indicate that when first admitted for some post-surgical trauma  he had whopping high LFTs and high-end VL of 2 million. Also pancreatitis.

- he recovers from the perforation and pancreatitis and is discharged. Six weeks later they seem him, quite possibly to follow up on the HCV, and lo and behold it's gone. Note that  LFTs, while still out of range are an oder of magnitude better. But they find another problem, with his thyroid, and start him on propylthiouracil for which documented side-effects are a reduction in white-blood cells.

- sure enough, by week 10 his leukocytes are way down and they stop the thyroid meds

- at the next follow up, week 21, the white blood cells are back in range but now the HCV-RNA is back! (140,000) and the LFTs are way out of range again

- the next two follow ups at weeks 28 and 47 show the hcv gone and everything back to normal.

Arguing for false results on the hcv-rna tests is pretty thin ice : the VL readings are whopping high values, not  borderline . More importantly they correlate well with the LFTs.  Of course none of this is conclusive but their conclusion that suppression of immune function by the thyroid meds led to temporary resurfacing of the VL at measurable levels seems quite sound. See also the other references of immune-suppression HCV rebound they cite.  "It is generally believed that hepatitis C virus is not completely eliminated from the body but is under control of the immune system." The fact that all this happened without the benefit of SOC seems to just underscore that the whole HCVhost "truce" is not limited to SVRs.


Perhaps the champagne fumes are still having an effect??

[mikesimon]

I have to agree with you - of course, you knew I would. Here was what I was working on to post to Jim:
While I am not necessarily disagreeing with your analysis I think that, assuming that your take is right, it does seem odd that this patient tested 2.3 million IU/ml at week 1, then negative at week 6, then 140,000 IU/ml at week 21, then negative at week 28 and negative again at week 47. You can call it quirky and/or acute but to see virus then no virus and then virus and then no virus seems noteworthy. We've seen no virus and then, upon relapse, we've seen virus back but, then it's back to stay. I am not including either false positives or perhaps a few virions hanging on - which we may have seen with a few members here. This guy's 21 week VL was 140,000 IU/ml.

I saw your response and stopped, seeing how much better you did than I was doing.

Be well and happy - both of you guys.

Mike

[jmjm530]

Nah, fell asleep before the ball fell, most be getting old. LOL.  

No, I think the acute stage -- and it is understudied because so few are caught in the acute stage -- taints this whole study, err case history. They simply don't understand the dynamics of how people clear the virus naturally. Does it happen all in one swoosh? Or does it happen in multiple swooshes? Also, I'm not sure if intermittent viremia during the acute stage necessarily means that the virus has to be high. Doc Shiffman explains it more in detail over at the Clinical Options site and btw these are not "false results" but rather viral behavior during the acute stage. Again, not aruging the whole occult thing here, just this one particular study.  But hey, now that the sensitive viral load thing has been put to rest, it's good we have something else to disagree about :)

Oh, how about a tiny link to the full-text free access. Thanks.

Be well,

-- Jim

[jmjm530]

meant to say in part "....I'm not sure if intermittent viremia during the acute stage necessarily means that the virus can't be  high at times such as presented here"

[jmjm530]

I'd have to take a look at the full-text, but will give it a stab anyway...

Given that the viral load went from DECT  (week 1) to UND (week 6) to DECT (week 21) to UND (week 28) and UND (week 47)...

Given these numbers, isn't it possible that what we're looking at is either: (1) one of a number of "normal" patterns in spontaneous remission, a phenomena that is studied nor understood all that well; or (2) that the introduction of this drug temporarily interferred with the pattern of spontaneous remission which was in progress.

In either case, I don't see how this supports the occult/persistent virus thesis because it's still unclear to me that the virus was entirely eliminated based on a single result of 140,000 IU/ml during the acute stage/struggle. As to the intermittent viremia -- a separate argument -- I would not call 140,000 IU/ml "whopping high" but think it could fit into Schiffman's thesis is intermittent virermia during the acute stage.

-- Jim

[willing]

Mike :  hey, I've always been a fan of the "reasonable man" standard. I'll be happy to sit on a jury with you anytime! Hope you had a good holiday are are well. My reservations about the cause have to do with the fact that the VL was detected almost 3 months *after* he stopped taking the immunosuppressants, but after all this guy was 69 - he's entitled to take his time.

Jim: OK, I'll poke around and see if I can dig up something about VL fluctuations in spontaneous clearance during acute stage (maybe that Scott Alaskan paper?)  but I'm fairly certain bouncing from UND to 2-million (over a range of 6 weeks no less) is *not* part of the normal process. Fluctuations in antibody rates seem well studied so presumably there's something about VL as well. However,   if that were the case I don't see how their paper would have gotten past peer review ( you can get the full text by clicking on the pdf icon in that link you posted)

[jmjm530]

Here's the Shiffman Slide Presentation -- See Slide 9 -- Free Reg required at Clinical Care Options Site:   http://webcasting.clinicaloptions.com/p41111200/

As to the "bouncing" -- isn't the 140,000 IU/ml  the only relevant number since that is the first Detectible following an UND.

Anway, as I thought I was clear in the first post, I'm not hanging all my hats on the intermittent viremia thesis -- maybe just the Stetson --- but hanging more of them on the understudied nature of the whole acute stage/spontaneous remission process, as explained in a previous post that might have crossed your last post.

-- Jim

[willing]

well I suppose it depends on your hypothesis about the underlying mechanism that accounted for the measurements observed. The study authors seem to believe the infection had resolved spontaneously by the week 6 test only to resurface on a week 21 test, quite possibly because of the immunosuppressant meds, and to then disappear again, permanently.

Your interpretation, if I understood it, is that the infection did not resolve spontaneously until at least week 26 and that the 2million,UND,140,000 readings prior to that are inconsequential fluctuations.  I couldn't see the data that backed that slide 9 from Friedman's presentation, however, the course of acute infection seems quite well studied,  though obviously there's less data on it that for chronic. See for example,

Kamal SM, Moustafa KN, Chen J, Fehr J, Abdel Moneim A, Khalifa KE, El Gohary LA, Ramy AH, Madwar MA, Rasenack J, Afdhal NH.

Duration of peginterferon therapy in acute hepatitis C: a randomized trial.
Hepatology. 2006 May;43(5):923-31. Erratum in: Hepatology. 2006 Oct;44(4):1055.
PMID: 16628640

In their study of 173 patients "with proven acute HCV infection", the overall spontaneous resolution rate was 23%, on target with expectations. Of these, none achieved spontaneous clearance after 14 weeks so assuming this guy only cleared after 21 would be quite a stretch.

It's just one case and there's no sense reading too much into it. However, unless you're inclined to throw it out as bad data, it supports the view that even for someone with the "right" CTL response, the virus persists and can be induced to rebound.

[jmjm530]

Willing: Your interpretation, if I understood it, is that the infection did not resolve spontaneously until at least week 26 and that the 2million,UND,140,000 readings prior to that are inconsequential fluctuations.
-------------------------------------------------------------
In part yes, except that I wouldn't consider the 2 million an "inconsequential fluctuation" since that was week 1 baseline, therefore only the 140,000 IU/ml and week six UND appears relevant as inconsequential fluctuations until an unreversable UND took place. True, the propylthiouracil was administered at week six with a following viral load of 140,000 at week 21, but this can be argued more than one way. The author's argue propylthiouracil-induced relapse, but equally plausible is that the acute process wasn't complete at that point and/or simply delayed by the propylthioracil in this elderly patient.

Willing: Of these, none achieved spontaneous clearance after 14 weeks so assuming this guy only cleared after 21 would be quite a stretch.
------------------------
The 14-week figure seems a bit short, but I'll have to accept it until I do some more digging. But note that this patient was genotype 3A who I believe have higher rates of spontaneous clearance and therefore might clear later than the 14 weeks stated.

But to a prev point, with most certainty none in the study were treated with propylthiouracil and developed leucocytopenia which could have changed the normal acute clearance curve.

I'll get back if I come up with more relevant acute studies. Thanks for the discussion. I mean, who really knows.

-- Jim

[jmjm530]

This letter from Berg may be of some interest in the unpredictable nature of RNA testing in the acute stage. While not matching up to the previous study -- a positive followed by an UND, then positive, then UND -- Berg does talk about postiives following negatives (viral relapse in spontaneous clearers) in a couple of patients where no prophlthiouracil type of treatment was present. Since we know that SVR is durable as measured in serum close to 100%, then these acute relapsers point out some of the differences between let's call it a spontaneous acute cure and a drug-induced chronic cure, suggesting that we can't make the "cure" call for an acute too quickly, as the authors of the first study apparently did in order to contrast it with what they contend is a  prophlthiouracil-induced relapse. No cure, no relapse.

-- Jim

http://www3.interscience.wiley.com/cgi-bin/fulltext/106595829/PDFSTART

[jmjm530]

"...(HCV Spotaneous) Clearance, if it occurs, usually happens within 4 months, but may take up to 18 months, or possibly even longer..."

http://www.hivandhepatitis.com/hep_c/news/2007/121107_b.html

"...Although viral clearance generally occurs within the initial 6 months of infection, recent studies have suggested that spontaneous clearance extends beyond this point.[7,34,35]"

http://www.medscape.com/viewarticle/521187_4

[susan400]

Short of a miracle, I'm not holding out for any spontaneous clearings of my HCV.  I've been chronic active for too many years now and I think its more likely to NOT happen, than to happen.  

Susan

[willing]

interesting points indeed, however:

- as noted in the reply to the Berg letter, and as is routinely posted here, SVR is durable but not impregnable. I know of no reason to assume the recovery obtained spontaneously differs in that respect from that obtained via tx. As  noted in the reply: the recurrence observed by Berg "appears to be an infrequent event" and "Viral recurrence may also occur after successful viral elimination by antiviral treatment.".

- Both the medscape article and the  "may take up to 18 months, or possibly even longer" summary by Liz Highleyman seem to refer to  

M Micallef, JM Kaldor, GJ Dore. Spontaneous viral clearance following acute hepatitis C infection: a systematic review of longitudinal studies. Journal of Viral Hepatitis 13(1): 34-41. January 2006.

a meta-study that simple collected previous publications. In turn their finding of prolonged post acute infection seems to go back to

Larghi A, Zulin M, Crosignani A et al. Outcome of an outbreak of acute hepatitis C among healthy volunteers participating in pharmacokinetic studies. Hepatology 2002; 36: 993– 1000

which tracked an unusual outbreak of HCV among volunteers participating in a study via in-lab PCRs.  As noted in the letter by Oldach accompanying that paper,

"It is striking that viremia was still detectable at 8, 13, and 24 months, respectively, in 3 of their patients who nonetheless went on to achieve spontaneous viral clearance."

On the other hand that recent Afdhal study I noted above, to avoid treating patients who might already have cleared, followed their patients quite closely to detect clearance point: "  To avoid unnecessary treatment of those patients who might achieve spontaneous recovery, all eligible patients were enrolled and screened for an initial observation period of 8 to 12 weeks. During the observation period, biweekly serum ALT HCV RNA analyses were performed"
and they observed "No patient in the no-treatment group had spontaneous resolution after week 14. Of the 131 patients who consented to therapy, 29 (22%) achieved spontaneous resolution of HCV infection during the observation phase and did not receive treatment. "

that is spontaneous resolution, when it happened, was by week 14 or earlier.

Overall, the Afdahl'06 and Largi'00 studies seem at odds. I tend to believe the former because of the larger sample, regular testing  and reliance on a well-calibrated  test (COBAS AMPLICOR TM HCV, version 2.0, Roche, lower limit of detection of 50 IU/mL), and OK , I just trust stuff out of Harvard.  However, I have to agree that Larghi'00 definitely raises the possibility of a much longer window for spontaneous clearance.

[sfbaygirl]

I remember HR saying it was not good to just stop interferon, it should be tapered. Since I had to stop ASAP, I didn't get to do this. Still afraid of the stuff!  

I know if I retreat with the same drugs, I will find someone to get me the Alina. Hopefully the VX will be around by then too.  Thinking about re treating is hard, I still get chills just thinking about doing this again.  John would kill me, so maybe I wouldn't last long anyway! lol  I like Jim's low VL statements. It would be great if my ins. would pay for lots of PCR'S  pre tx.  

I haven't read the whole thread yet. Wow is it long.  I guess I won't be bored tonight!  

All of us relapsers have a tough call and I hope we all SVR soon!  

Best to all!
Linda

[sfbaygirl]

Interesting thread...but since most of us are way past that acute stage, I had to skip some of it.  Wish I had tx'ed then,  but there were no tx's when I was acute.  

Just wanted to add to my list of what I would want next tx.  I would double dose, besides tapering.  Get rid of those virons quickly at first. I think this is important, perhaps my take, but it is.   I wasn't clear at week 12, had a VL of 6 mil. It is the same now and when I relapsed.  Not sure I would want to do the infergon route,  but maybe.  I am layed out on tx anyway, why not?  When I saw HR, he went into more detail about tapering.... I would do this. There are ways to get Alina from other countries, while expensive, I would sure do it if I could.  

BT; So sorry about your relapse!  Susan;  you hang in there girl, something will come along to get you to SVR.  

Hugs to all!
Linda

[Mr Liver]

I am sorry to hear of your relapse. I'm on the waiting list and needless to say this circumstance is of great concern to me. I have failed tx twice and I am hoping newers meds will come to my rescue,as well. I wish you well and I hope the newer meds can make a difference for all of us who need something more that SOC.
regards,
Mr Liver

[willing]

OK,  as a fellow relapser,  it's my turn to get my a** off the bench and do a little cheerleading dance. True that this past year was somewhat of a  disappointment on the new drug front. As someone waiting  for combo tx that includes  both  protease and polymerase inhibitors I'm not sure '07 made any reduction  in my projected 10 year wait. However...recent progress on the anti-fibrotic front is really impressive.

Focusing on eliminating the virus can get compulsive but is a bit like obsessing over a bad video game. If fibrosis is sufficiently contained, there's a reasonable chance one can happily cohabitate with the virus indefinitely...and while that road is not as straightforward as signing up for soc, there are pretty good indications to follow per hr's recent posts.

[BThompson4]

Thanks everybody for your encouragement.  I've had hep c 35 years, and though not always very good times, my new liver is still in pretty good shape (F1 fibrosis) seven years after transplant.  I am blessed to be in this position, having seen a couple of  friends' transplanted livers eaten up quickly by the virus.

Mr Liver: maybe your new liver will do better than the old one with a future tx with SOC or a new cocktail .  I used to be kind of upset that I got an "old" liver at transplant (I am 52; the liver is 60); but the transplanted liver sure did respond nicely to only 36 weeks of SOC (went from F2 in June 2005 for F0-F1 on March 6, 2007,  which was week 36 of treatment).  This disease can have unpredictable outcomes.  I hope you have great results with your new liver!