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151263 tn?1243377877
SVR Eradicates HCV
Not sure if this has already been posted, if so it bears repeating:

http://www.natap.org/2008/EASL/EASL_77.htm

"SVR Eradicates HCV

SUSTAINED VIROLOGICAL RESPONSE IS ASSOCIATED WITH ERADICATION OF HEPATITIS C VIRUS AND DECREASE IN ANTI-HCV TITER IN PATIENTS TREATED FOR CHRONIC HEPATITIS C

Reported by Jules Levin
43rd Annual Meeting of the European Association for the Study of the Liver April 23-27, 2008, Milan, Italy

M. Martinot-Peignoux1, S. Maylin1, N. Boyer2, A.C. Cardoso1, M.P. Ripault2, N. Giuily2, C. Castelnau2, M. Pouteau2, P. Bedossa3, P. Marcellin1,2 1 INSERM, U-773, Centre de Recherche Biomedicale Bichat-Beaujon CRB3 Hopital Beaujon, Clichy, 2 Service D'Hepatologie, Hopital Beaujon, Clichy, 3 Service D'Anatomie Pathologique, France

ABSTRACT

Background-Aim: Hepatitis C virus (HCV) eradication, in patients with chronic hepatitis C who achieve a sustained virological response (SVR), is still controversial. In this study performed in patients with chronic hepatitis C who achieved an SVR, HCV-RNA was measured in serum, peripheral blood mononuclear cells (PBMCs), liver and anti-HCV antibodies titers were assessed, during follow-up.

Methods: 278 patients with an SVR after treatment with IFN alpha-2b or PEG-IFN alpha-2b+ribavirin, were studied. HCV-RNA was tested: in serum for all the 278 patients every year and at the time of PBMCs or liver collection; in PBMCs in 71 patients 3.9±3.4 (0.5-10) years after treatment; in liver 38 patients 3.2±1.6 (1-5) years after treatment. HCV-RNA was detected with the VERSANT HCV-RNA Qualitative assay (TMA). In 142 patients HCV antibody titers were measured with the Axsym HCV 3.0 (Abbott), and with the third-generation HCV recombinant immunoblot assay (RIBA) (CHIRON RIBA HCV 3.0 SIA), before therapy and 4.7±2.2 (0.5 to 11) years after treatment. Liver histology was assessed in 92 patients with paired biopsies 1.4±1.9 (0 to 10) years.

Results:

Patients were followed up for a mean of 3.5±2.4 years (range, 0.5-17) years.

Serum HCV-RNA remained undetectable in all the patients (1050 samples).

None of the patients had detectable HCV RNA in the PBMCs or in liver.

The mean anti-HCV titers were 93±19 IU/ml and 45±21 IU/ml, before therapy and on the last serum sample available, respectively (p < 0001).

The most significant decrease was observed with anti-NS5 antibodies (p = 0.001); anti-c22 antibodies remained unchanged.

Normal serum ALT levels were maintained in 94%, fibrosis stage was improved in 57%, stable in 32%, deteriorated in 11% of the patients.

Regression of cirrhosis was observed in 7 of 10 patients.

Conclusion:

In our 278 patients with chronic hepatitis C and SVR, evaluated up to 17 years after treatment cessation, none demonstrated late relapse or the presence of HCV RNA in serum, PBMCs or liver.

HCV antibody titers showed a marked decrease. These results demonstrate a durable response to IFN alpha 2b or PEG-IFN alpha-2b+ribavirin and indicate that SVR is associated with HCV eradication and progressive decrease of anti-HCV."
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I agree with your comments and reference support cited above.  Its hard to discuss or debate an issue like this, especially when the scientific research that one offers to support a point of view is either dismissed as inaccurate or ignored by other parties...but at the same time any research studies offered up on their end are expected to be taken as the 'last word', and accepted as absolutely valid, without that same chance of error, or oversight that are applied to your reference studies.  I have pretty much given up debating many of the issues that are sometimes considered controversial because no matter what you might offer up in support of a view it is generally dismissed as invalid, subjective, biased by contamination, or worst of all, based on one's own 'paranoid' point of view regarding the virus.  If all else fails in an argument, then the final resort in discounting the person debating the other side is to just label their position as wacky!

There has been little or no scientific explanation for the many research studies using more extreme amplification of the virus which have shown low level REPLICATION years down the road after SVR.  I am interested in what this might mean, rather than trying to just explain it away with my own conjecture.  I also get a bit irritated whan people refer to the 'toxins' washing out of our bodies after tx, and that the interferon slowly stops 'poisoning' our cells over a long period of time, which supposedly explains post-tx problems.  The fact is that interferon just up-regulates our entire immune response, thus causing our systems to go into a sort of hyper-immune-overdrive mode during tx.  Some of this immune re-regulation does not just 'go away' after tx, even though the interferon itself is gone pretty quickly from our bodies.  Rather than having 'toxins' hanging around in our cells over long periods of time, we are really seeing a system that has been jolted and stimulated, and that does not easily go back to its former configuration quickly or easily.  For some people these abberant, often disruptive and painful reactions remain for years, for others their immune systems rebound to more or less normal in a few months.

I really appreciate your calm perseverance, and point by point dispassionate response to the debated issues above.  I find it harder and harder to exercise that same degree of patience these days, and hence involve myself far less in controversial debate.  I have felt the frustration of presenting research, logical points, and supporting data only to see it either ignored, or just discredited as 'faulty' with no scientific support from the other parties, or proof of just why its not accurate.  At the same time we are asked to take any studies supporting the opposing point of view, no matter how unsophisticated or isolated, as proof of point, end of discussion, etc.  

I prefer open minded discussion, and am more than willing to modify my beliefs and positions if someone can scientifically show my why I should, and explain why the studies I might cite are as absolutely 'invalid' as their studies are 'valid'!  

I hope you are well, and enjoying life.  I am very much, and have been doing a good bit of world travel with my family, interspersed with running my business.  In spite of the downside of post-tx life, I find that overcoming obstacles, and enjoying the positive stuff is still my forte.  Thanks for your always extremely lucid discussions, and the absolute calm rational approach that you bring to the forum.

DoubleDose
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151263 tn?1243377877
You didn't respond to the vast majority of what I said above, so I think it's pretty obvious at this point that you are unable to accommodate the factual observations carefully described above (that tend to cast significant doubt on viable/reproductively active viral persistence). It's also obvious at this point that your mind is made up and you believe in viral persistence (which is certainly your prerogative). I also notice a pattern of behavior of only referencing studies that support your point of view and omitting studies that would tend to contradict or cast doubt on this view. Nothing wrong with that either, I just had previously thought of you as being more dispassionate and non-biased about the whole "creepy crawly" thing (as opposed to DD, for instance). I won't bother discussing it further, other than an obvious response to one of your last comments:

">this sounds like the wildest conjecture. I’ve never heard any such thing.>>   how do you think people get to SVR via SOC? unlike PIs, IFN/RBV have no toxic effect on the virus (one can quibble about the RBV) they  simply stimulate anti-viral pathways. Improvement of the immune response, via stronger HCV-specific CD4/CD8 cells etc. etc. is the whole point of SOC.."

Of course I think people get to SVR via SOC via the immunostimulative and possibly directly antiviral effects of SOC. But, clearly and very obviously, those effects are temporary, and only work as long as you keep taking the drugs (that's why many people achieve and maintain UND status during tx, only later to relapse once the drugs stop). But, again obviously, the point here isn't what happens during tx, the point is what happens after tx when SVR is achieved. That's why the title of this thread is "SVR eradicates HCV", and that's what we we've been talking about all along. Your conjecture above was our old friend the "quarantine" theory (an old favorite of DD's). Except you didn't call it that, you called it "improvement". You inferred that the immune system is "improved" *after* SOC treatment and so improved that it contains or quarantines the virus permanently afterwards due to its "improvement." Even in the face of all kinds of conditions and challenges to the immune system. You fail to provide any information or evidence or data to substantiate this improvement, nor do you explain how this improvement process takes place in tx failures and SVR's, nor (once again for the 4th time) did you address (in any way) the *very* obvious and devastatingly pertinent facts concerning SVR durability in the face of disease and drug induced IMMUNOSUPPRESSION. I think at this point it's fairly obvious you're not taking that one on because it doesn't fit into the "big picture" as you see it (as explained above). But like it or not, it *is* a part of the big picture, and all the blinders in the world will not make it go away.

And DD - please, accept that the creepy crawlies are a part of your world. Accept that they're in your eyelashes right now. Accept that they're coursing through your veins and running through your gut. Accept that they're in your bed and in your brain. They're *there* dude. They will always be there and there's nothing you can do about it. We are a part of a much larger ecosystem; we ourselves *are* an ecosystem in and of itself. Zillions upon zillions of hitchhikers are around us, on us, and *inside* us. Many for our own good, many we owe our very survival to! Some not there for our own good. But just as we live parasitically off of plants and animals, and take what we need from the ecosystem to survive and prosper, we have creepy crawlies that do the same to us. And they'll feast on us, buffet style, when we die too. But you know what? It's all good, it's all good dude. It's all a part of god's plan, pilgrim. So be well and accept your place in the universe. Because you're gonna drive yourself nuts fighting the creepy crawlies dude...and I mean flat out bonkers man. Please, turn back before it's too late. If nothing else, do it for the children! ;-)  And always remember: COOTIES REIGN SUPREME!
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Am I the only one who sees one side drifting more and more into the "argumentum ad hominem"? It's really becoming more and more predictable and more humorous too - arms flailing wildly in the air.
I'm not certain about this SVR issue by any means and I wonder how someone can appear to be so sure about this. But I do have an opinion about see who is winning the argument here - it's willing with his hands down, sitting calmly amidst the tempestuous sea of desperate insult and innuendo swirling around him .
Mike
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I must admit that I'm enjoying a bit of the ad hominem directed at both Willing and DD, as both have directed some at me in the past on this same topic, and same with you my friend, on other topics --  so I guess you all were losing your arguments with me? LOL.  Ad hominem aside, I think good non-ad hominem points have been made on both sides. Job well done, fellows.  One of the better discussions on the issue to date, so thank you to the participants.

-- Jim
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BTW my take (and my liver specialists), as expressed before, is when the virus is gone, it's gone -- at least in a *meaningful* way. And until whatever it is that some researchers repor they see under a microscope/centrifuge are given some clinical signficance, I'm not going to lose much sleep over it. Yes, in the words of "Mre", the "cooties" are all around us, so as long as they leave me alone...
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I would likes to see where willing resorted to an ad hominem argument with you or anyone else for that matter. Me? I can believe that about me easily but willing? I haven't seen it ever from him. Mike
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I think we all - or the vast majority anyway - agree that SVR means it's gone in a "meaningful" way. I cannot speak for DD on this point but when I see normalized liver enzymes, undetectable viral load and improved histology that sure looks meaningful to me. And durability is a big plus too. But, that really wasn't what I thought this thread was about.
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232778 tn?1217450711
If it is gone in a meaningful way, why is this research important? Why are some researchers saying it is completely eradicated, and other researches stating otherwise? It is either gone, or it isn't. Some think it is, some think it isn't. I'm inclined to "think" it is gone, and the arguments above I think, on balance, support that view, particularly as it matches peoples experiences. IMO the odds are that this is a research / testing issue rather than a medical misunderstanding about some mysterious property of Hep C that may or may not exist, whereby Hep C can change such that it is not Hep C, or whereby our bodies are magically stronger at containing after treatment. In saying that, I might be wrong, but for me, I'm happy with the eradication research which is a highly plausible and compelling hypothesis, and find the thread an interesting read - not disturbing at all.
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151263 tn?1243377877
Don't worry jim, I can handle the viral persistence club as it adjoins the back patting DD/willing/mikesimon clique. And although there may be some saucy words exchanged here, make no mistake - bringing up these incredibly obvious, plain as the nose on your face issues is absolutely salient, pertinent, applicable, within scope, exactly on target and exactly on topic. Nothing ad hom about it mikesimon. And for you of all people to be the ad hom policeman around here is a joke anyway. If you don't like what I have to say, feel extremely free to SKIP IT, bub.

I just find it amusing how there are a couple of self appointed experts around here on viral persistence who have begun to carry themselves as if "the argument's over", or as in DD's case constantly coloring himself as the noble, besieged, objective and scientific inquirer who just "wants to get to the truth" but is constantly unfairly attacked and dismissed by a moblike horde of doubting idiots. I usually skip over these persistence threads because I really don't care that much about it. I don't obsess over it like DD and a few others do. I don't have a file catalog with every study done on it that just happens to agree with my preconceived notion that it's already true (leaving out reports like the one on this thread's heading). And I don't sit around just waiting for another thread that even remotely pertains to the subject to come around so I can weigh in with my "expertise" on the matter (often scaring newbies with the concept that you're "never really cured").

So just this once I thought I'd probe into this issue using some common sense inquiry and very basic observations with "the experts" and see if they could teach me something I didn't already know. Well, big surprise - isn't it funny how they really don't know much about it at all? They don't have any answers to these perfectly reasonable questions, but yet they're still "the experts", with the implied swagger that the argument's over when it comes to viral persistence. Unless there's someone else out there reading this that knows a lot more than you guys do about this subject, sure sounds like the argument's FAR from over to me.

So in the meantime guys, stay away from those cooties. Except DD of course, he won't be able to - but at least give it the 'ole college try?? ;-)
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I have been undetectable since April 2003 and I stopped treatment in June 2004. I have tested every month since I became undetectable with Heptimax test < 5 IU/ml.
I have a biopsy report from June 3rd 2006 which shows a low VL HCV.
I go to a very well known and respected transplant canter and the chief pathologist is a world renown expert.
How do you explain that? Misread biopsy perhaps? Wrong PRCs every single month for 2 years - one just 2 weeks before and one  10 days after my biopsy and both were undetectable. Maybe we transplant recipient SVRs are unique and just happen to show HCV on biopsy.
I know I was very surprised when I learned of the biopsy results.
But, my surgeon wasn't the least bit surprised - he's seen this stuff before because he sees a lot of biopsies - even SVR biopsies. How many SVRs do you know who've undergone a liver biopsy post clearance?
By the way, my surgeon says that he has had SVR patients who showed no sign of HCV anywhere with any test and you know what he said? He said he sees a higher than average incidence of acute cellular rejection in these patients. Must be immune system related somehow.
Mike
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I just figured it out - the biopsy showed HCV because of contamination.
Of course!
Mike
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It's hard to say what to make of that, or what was picked up, especially because when you were asked a year or so ago some specifics of that test you replied that you had failed to ask the surgeon and btw my "renown expert" believes once the virus is gone it's gone for all practical purposes. In any event, sure glad that whatever that single test showed, you're back to UND. Of course, one explanation is that with all the sensitive testing you get that one every blue moon is bound to be a false positive, and frankly that's why I don't test any more :)

-- Jim
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As to your surgeon seeing "a higher than average incidence of acute cellular rejection in (SVR)  patients -- yes, it could be the immune system still over-primed by the interferon from SOC per this paper here:

http://www3.interscience.wiley.com/journal/109085972/abstract
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Don't worry, our flailing, and foaming brigade will find a way to dismiss your case and your highly experienced surgeon's opinion as not relevant.  Or they will just plain ignore the implications.  Far from obsessing over 'persistent' virus, as our colorful friend would claim, I am not on the forum day after day ranting and raving over everyone elses opinions and research comments.  I am pretty much living and enjoying life.

I continue to be interested in the significance of 'persistent' virus as demonstrated by now numerous studies, and even acknowledged by many researchers and growing numbers of hepatologists.  Not because I am obsessed, because in reality I think about it very infrequently, but sometimes when I come back to the forum and see long-winded, insult ridden, conjecture laden diatribes, I just can't resist throwing in my own two cents!  Whether I am right or wrong in my opinions on HCV, I can tell you one thing I am dead sure of, and right about:  some people make a complete farce of the concept 'intelligent discussion' regularly and repeatedly.  It doesn't do much to further the aims of the forum.  In my opinion it just promotes more antipathy and displeasure with reading the threads.  

This is why I don't like to spend much time or energy on these threads anymore.  If you have to wade through constant reams of personal insult, emotional venting, and ridiculous accusations....why bother?

I really do appreciate that there are a few cooler and calmer heads here that can digest and wade through the garbage, and manage to maintain a very mature, respectful, and objective demeanor.  (I am not including myself in this comment)

One final thought regarding 'viral persistence', I will say again that I agree with the 'durability of SVR' consensus opinion, and the 'repair of damage' potential for SVR, and even the concept of 'virtual, or effective' viral disappearance'......my concerns with the possibility of, and growing evidence of persistent replicating virus have more to do with the possible effects of keeping a virus in 'remission' by our immune systems (if that indeed is what is taking place), and the long term possibilities of 'reservoir virus' slowly causing changes in the functing of our CNS, or brains.  Much of the study on those who 'spontaneously recover' from acute HCV infection shows that the great majority of these people continue to demonstrate typical HCV extrahepatic symptoms, decades after the 'spontaneous resolution' of their initial infection.  The scientist in me really needs to fully understand why this happens, and whether it has to do with 'viral persistence', and related issues.  

We do know that 'occult HCV' (different than persistent virus) is becoming found more frequently in a number of people, and this alone also indicates viral behavior contrary to current explanation.  The doctors and researchers don't really understand how any of this happens...but apparently they should call Mremeet and get some solid answers to their concerns.  They will be very gratified to know that we have such a prescient specialist in our midst!

Have a great week guys (and gals), and remember to ENJOY!

DoubleDose
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151263 tn?1243377877
"Have a great week guys (and gals), and remember to ENJOY! "

I'll sure try. But, how is that possible with all these cooties all over us? Hey, why don't you check out this song and start the weekend early with it? It's *all* you dude...

http://youtube.com/watch?v=X--QWXGjXfg
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You are right on one count:  He is the MAN!
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HA HA HA lmao... great ending!

jasper
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DD:
thanks for the update; very glad to  hear you're doing well. If you can handle long-distance flying and still feel well I'd say your health is way ahead of the median..

moahunter:
>If it is gone in a meaningful way, why is this research important?

(1) in-depth understanding of how hcv interacts with the immune system, even beyond SVR,  is of value in vaccine development and in tx design for non-responders/relapsers (2) you learn a lot about how something is put together when it breaks; HCV breaks our immune response in fundamental ways, it has a lot to teach us.

mremeet:
>You fail to provide any information or evidence or data to >substantiate this improvement, nor do you explain how this >improvement process takes place in tx failures and SVR's,

if I'm understanding you correctly, you're questioning whether control of the virus could be due to an improvement in the immune response? But that's precisely what adaptive immunity is all about!
See the wikipedia article for an introduction:
http://en.wikipedia.org/wiki/Adaptive_immune_system

Development of strong HCV-specific, antigen presentation and CDC4+  CD8+ Tcells is the crux of immune control. From a recent review out of Harvard (yeah, I know, more ad-hominem name dropping)

http://www.ncbi.nlm.nih.gov/pubmed/18514579

"CD4+ T cells have multiple effector functions in antiviral responses,
both via secreting antiviral cytokines and via activating
viral specific B cells and CD8+ Tcells. A strong preponderence of
evidence demonstrates that in the acute phase of HCV infection,
vigorous, broadly directed and sustained HCV-specific
CD4+ and CD8+ Tcell are closely associated with a self-limited
course of infection [26,84–88]. HCV-specific T cell responses
and the induction of IFNγ in peripheral blood and liver coincide
with a decrease in HCV RNA titers [26,30,89], although there is
a notable lag between the onset of viremia and the onset of T
cell responses [26,89,90]"

A free-access overview is:
http://www.ncbi.nlm.nih.gov/pubmed/10790425

The 'strong preponderance' mentioned above is primarily in the context of acute; there's not yet as much data distinguishing successful vs failed tx on the basis of CD4/CD8 profiles but it seems a likely extension.

> nor (once again for the 4th time) did you address (in any way)

I did, it was buried in the 'etc.etc.' fine print regarding conjectures. Maybe the impregnability of SVR even in the face of  immune-suppressive medication supports absence of viable virus; equally plausible is the conjecture that the suppression is nowhere near strong enough to cause resurgence (did you develop any major bacterial or viral infections while taking that 80mg of prednisone?).  And again note that there *is* some, though scant,  documented evidence of resurgence as posted above. However, there's not much point arguing about this - it simply isn't direct evidence, pro or con.

>your mind is made up and you believe in viral persistence
..
>only referencing studies that support your point of view
not so - as noted above, in addition to Maylin'08 there are two other recent studies that report no finding of post-SVR HCV RNA in PBMCs (and all three failed to apply mitogen stimulation of cells prior to PCR). The list of research TN has compiled on the 'occult' health page speaks for itself. If you believe it's one-sided you should extend it; I'll be surprised if TN has missed much.

And BTW, his  most recent addition (Hoare'08, he now seems to be adding pre-prints even before publication! you'd think keeping that hair-do in shape wouldn't leave him much time) concludes with

"Non-viremic HCV-antibody positive patients have a liver biopsy that is usually abnormal. Fibrosis was present in most with similar inflammatory infiltrate to viremic cases. The presence of a  CD8+T rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV-RNA negative cases"

None of these patients had undergone tx, their HCV-RNA und status is due to their unaided immune respose. However, as I recall, you were arguing a while back that all SVRs are created equal..
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Careful quoting that study. When i did further up the thread, the data was considered too old to be meaningful as it was before the Peg/Riba era.

Ok i thought he missed the point, but hey If he wants to believe that so be it.

CS
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sorry, but I didn't understand your comment. Both quotes in the preceding post are  from recent articles. Ishii'08 is

Immune responses during acute and chronic infection with hepatitis C virus.
Clin Immunol. 2008 Aug;128(2):133-47. Epub 2008 Jun 2.
PMID: 18514579

and Hoare'08, the most recent addition to the 'occult hcv' health page, is

Histological changes in HCV antibody positive, HCV RNA negative subjects suggest persistent virus infection,
Hepatology, (still pre-print)
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Yeh i know it is. I used that study earlier and this was a response

"172 HCV-antibody positive, serum HCV-RNA negative patients underwent diagnostic liver biopsy between 1992 and 2000 "

That study was before the current Riba and peg protocols (almost 16 years ago) so it is not surprising that the results are more negative.

The studies that  and Mike present are within the past few years and both indicate that viral RNA was found in less than 2-3% of the patients after five years.

I'm calling that a cure (personally ) and hope that it works for me!  :)

So I was kind of having a dig back at the poster not you.
And i still think he missed the point

CS
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I think we can just examine the phrase that is used for successful HCV therapy to understand where the medical community is leaning on this issue:  Sustained Viral Response.

It means the virus is at undetectable levels on standard PCR testing, and remains so over long periods of time, possibly even permanently.  The response (to undetectable levels) has been sustained (ongoing).  What the term does not state is: Viral Eradication.

This all gets back to the meaning of "IS" as Bill Clinton would have said...or in this case the meaning of 'cured'.  We have all had this discussion many times, with tons of supporting argument and research on all sides, so I won't rehash any of that.  I will just say that 'cured' is what SVR now implies, but the meaning of that 'cured' ranges from the concept of 'pushed to undetectable levels on a permanent basis, to at the other extreme, 'totally eradicated from the entire body, and gone forever with no low level replication or compartmentalization'.

I do note that most of the Liver Association, and Medical Advertising literature still hedges the bet considerably by stating in small print that successful therapy causes the virus to 'remain at undetectable levels'.  I always get the feeling that none of them really feel comfortable using the word 'eradication' for fear of down road research findings, or possible litigation, etc.

So, in summary, we do have a cure, but lots of disagreement over the finer aspects of what it consists of.  Many of us continue to be concerned about these issues chiefly (I believe) because so many of us still experience a host of post-tx, post-SVR issues that seem strikingly similar to the pre-tx HCV symptoms.  We want to know if the possibility of having 'persistent viral infection' after SVR could be a reality as much research testing has discovered, and/or could be one of the causes of post-tx problems.

I hope these comments spark no controversy, because that is pretty much how things are in the HCV world today.  I don't think that ANYONE has concrete, final, immutable proof or answere, one way or the other.  Now the fact that Dr. BigReputation says that SVR is in his opinion equivalent to Total Eradication, means no more than another professional opinion, in a sea of conflicting research and other opinions.  I respect the opinions of both sides, but consider them only 'opinions' until finally proven and agreed upon by all leading HCV medical experts and reputable HCV researchers.

That's MY opinion, anyway.

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I thought I was going to have to bump this thread back to the top with my admission that I was mistaken. It's really not any easier but perhaps it is providential that there has been recent activity in this thread.
I have been operating under the assumption that molecular testing of my tissue sample detected active HCV. My biopsy was a little over two years ago and I thought that I understood the methodology - at least from a layman's limited understanding.
I have been in touch with the chief pathologist at the lab which processed my biopsy and he told me that no additional testing was done on the tissue sample to detect HCV. He said that the author of the report assumed that I had active HCV because that was my underlying disease which necessitated transplantation and he saw some inflammation and fibrosis in the tissue sample which is characteristic of HCV. Basically the report said:

"Well you had HCV pre-transplant and we see inflammation and minor to moderate fibrosis in the tissue sample so we're calling it active HCV".

That certainly doesn't rise to the level I have come to expect from my center and it is somewhat disappointing. But, the bright side is that I suppose that I can once again seriously entertain the idea that I am HCV negative - and that is somewhat comforting. I have never been invested in believing one way or the other. My opinions are driven by information and even when the information isn't favorable I try and keep an open mind about it.

So,

MY BIOPSY OF JUNE 2006 DID NOT SHOW ACTIVE HCV AND ANYTHING I HAVE SAID UNDER THE ASSUMPTION THAT IT DID SHOW ACTIVE HCV SHOULD BE DISREGARDED.

I apologize for not knowing what I was talking about here. Of course my situation doesn't explain the Tram, Pham and Casitllo arguments but neither does it support them.

Mike
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Thanks for taking the time to double-check on what your liver molecular testing actually showed. In all fairness, you did state back then that you weren't sure of the exact methodology used for those tests, and it was others that seemed to run/extrapolate  your anecdotal report more than yourself. Of course, the really good news for you -- and hopefully for all of us - is that they did not find HCV in your liver tissue.

If memory serves me, weren't you put on a short course of interferon after that report read? If so, and if it was based on a false read of that report, I'd be a bit ticked off, but maybe I have things a little off, it's been quite awhile since you posted the incident.

-- Jim
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I did follow up on my biopsy and after reading closely the disclaimer which mentioned molecular testing I assumed that was what was used. I also discussed it with my transplant coordinator and she seemed certain that some type of staining was done which detected HCV.
After my biopsy I was put on half dose Pegasys, low dose Ribavirin and increased Prograf (anti-rejection) dose. At the time it seemed like the shotgun approach where you shoot at everything and hope to hit the target. I will say that the chief pathologist acknowledged that there is a possibility that there is active HCV in my tissue sample and that my stimulated immune system anti-HCV attack was responsible for the enzyme elevation. This acknowledgment was not in response to a question from me or any prompting by me. He just listed it as one of two possibilities and, in doing so, stated that some patients with undetectable serum show active HCV per tissue PCR on biopsy. He suggested that if I have another biopsy I should request a tissue PCR which "will help determine whether the treatment has resulted in viral clearance or viral control". He also stated that this is a very complex situation. I think I already knew that.
The other possibility he mentioned was that I "had a minor component of rejection" and that caused my enzyme elevation.
His one statement which is most relevant to this discussion was:

"Negative serum HCV RNA testing does not mean that the liver tissue is negative for HCV".

I trust this man on this issue so I believe that negative serum testing is not necessarily the final word on this "eradication" issue.

As to what happened to me in 2006? I would have to bet I had some degree of organ rejection. It could have been HCV and my immune system but, without evidence of active HCV, I think rejection is the more likely culprit.

Mike
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Couple of quick questions:

- When you had your initial possibly/probable rejection episode (2006), did your serum levels show any detectable RNA?

- You mention above that no PCR was performed on the resulting sample from your '06 bx. Wouldn't that then leave the question open as to whether your liver is RNA+ or -?


Hopefully, it will turn out to be the case that you are hep-neg. When will your next bx be? And do you plan on asking for a PCR to go along it?


Hope all is well with you and family.


TnHepGuy
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No - and I was tested 1 or 2 weeks before and 10 days or 2 weeks after. I would have to check to be precise about the time but both the before and after were absolutely positively within one moth of my biopsy.

Yes, there was no PCR or molecular testing of the tissue sample so that question is up in the air - whether there is any active HCV in my liver.

I don't know when I want another biopsy. It's not the procedure that scares me - it's the results. My enzymes have been consistently in the low teens since they normalized and I get a whole lot of labs - every two weeks. So I think I have a clue about my liver healthy without a biopsy.
But, when I do get one you can be sure the tissue sample with undergo PCR testing - without question.

All is well on this end and I hope that you and your family are well also.

Mike
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Your comments are really good news, especially from your personal perspective.  In the few studies that I have read regarding positive hepatic virus and negative serum virus, after treatment, I do believe that the LFT's were somewhat abnormal in the liver positives.  I can't imagine that with LFT's consistently in the teens that you would have active or chronic virus in the liver.  You sure have a great shot at good news, anyway, since you had no PCR of tissue, and now understand that there was no confirmation of active virus other than some circumstantial inflammatory signs in the liver tissue.  I would think that to be probably typical.

I do think that the issue of persistence probably is a little different from the issue of positive/ or negative hepatic tissues after SVR, in that I would think the persistent viral matter would be sub-detectable (if there is any actually there), and would need extreme amplification to detect.  It would likely be in various other organs and tissues as well.  The real question ends up being one of 'accurate PCR test results with true low level replication, vs. some other manifestation or contamination that shows up as 'replicating virus' on extreme PCR amplification.  I am uncertain if either position has much certainty at this point, which is why I remain open to final determination by scientists.  Although some of us are said to be in the 'viral persistence' camp, I would characterize it as the 'open to the concept of viral persistence, as research has frequently suggested' camp.  At the same time I sense that others are in the 'absolutely sure it is eradicated, and totally cured' camp.  That is just fine with me, and it is their right to hold that opinion.  In fact, I really hope that they are right!

I think the issue of liver infection, with a positive PCR using ordinary testing is another subject apart from 'persistence' and may be related in many ways, or more similar to Occult HCV, or they may all be manifestations of the same thing, just moving on a continuum from very invisible to very obvious.  

I hope that when and if you do the biopsy/ PCR that you end up seeing only a big goose egg!!!  I think you will!  

Thanks for the candid retraction and clarification...it puts everything in a much nicer light for you, and for us!  Your surgeon does seem to see the possibilities for different viral outcomes, and SVR behaviors, and that in itself is another red flag waving toward the need to further study 'occult', AND 'persistent' HCV.  I believe this, anyway.

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CS : thanks for the explanation; yes, given that the study is reporting results on patients who had never undergone tx,  SOC protocols seem irrelevant to the findings

all: interesting twist in a various ways : the assumption that the inflammation is HCV-related and the pathologists' comments, however,  on a personal note, it's got to be good news!

The discrepancies between what reputable specialists have to say on the topic underscores for me that the issue is still very unsettled, hence the ongoing controversy  on this forum and in the published literature is not idle bickering.

Personally I tend to give more credibility to those working at the lab-bench/microscope, like Mike's pathologist, than to clinicians, like Jim's specialist, who work further downstream (for many Dr's, the personal definition of cured probably comes down to the fact that they never see SVR patients again).
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Willing:...l ike Jim's specialist, who work further downstream (for many Dr's, the personal definition of cured probably comes down to the fact that they never see SVR patients again).
---------------
Actually my specialist works at the main pond and I'm still seeing him two years after SVR. Do watch out for those oats btw, they can make you stubborn as a mule :)
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My surgeon thought it was HCV before even seeing my biopsy report - just by seeing the enzyme history.

I really don't know what to think about me and HCV. I can tell you that I was really surprised when the chief pathologist gave me the story. I just wanted to know the specific molecular test that showed HCV. I was floored when he told me there was no test. If I gave you the pathologist's name and you Googled him you would be amazed at how much he publishes and the complexity of topics he addresses. This man is one of the preeminent pathologists in the country so when he told me that "negative serum HCV RNA testing does not mean that the liver tissue is negative for HCV" I have to believe that he has seen it in his lab on more than one occasion.

To be clear about this I never asked my surgeon this specific question. I haven't even seen him since the biopsy results so I cannot say that he intentionally or negligently misled me. Maybe hes seen so many serum undetectable patients show HCV on biopsy that he just accepted the results as accurate. When I first posted the story about my biopsy Jim and willing wanted to know what test was used and I started investigating. When I saw the disclaimer regarding molecular tests which were not FDA approved but were developed at my center I figured that one of the listed tests was the one that was used. At the time willing and I were in touch with one another and it was willing who called my attention to the fact that immunochemistry-based detection of HCV proteins in biopsy samples is possible and that the language on my biopsy report contained references to those types of tests. That's what I thought the pathologist was going to tell me - which specific test was used. Suffice it to say that I am not happy about this. Since I have been serum undetectable since 2003 and stopped TX in June 2004 I think a PCR of my liver tissue in June 2006 would have been more than reasonable - it should have been mandatory. My surgeon was out of the country when the biopsy was ordered so I can't necessarily blame him for the order although I don't completely absolve him of responsibility either. But after he saw the results he should have sent me immediately to get another biopsy with a tissue PCR to be certain about what was causing my enzyme elevation. There's nothing to biopsies as far as I'm concerned  - except the results that is. I really don't know exactly how many I've had because I have had a bunch. And they sure aren't anything to the surgeons - they order them all of the time at the drop of a hat. I think a PCR should have been done on my tissue without question. The fact that it wasn't does trouble. I am reminded of what my surgeon told me just 2 or 3 days after my transplant. He said "don't trust anyone" and I replied "except you, right?" and he said "no, not even me". It does seem that the older I get and the longer the relationship the greater the likelihood of disappointment. If I have learned anything through this is that my surgeon was right when he told me not to trust anyone. And the mistake I made was to trust. When my AR dose was being reduced (it was a weaning off process of all AR drugs) I thought that the reduction that triggered my problems was too drastic. I also thought that testing every two weeks following the dose reduction was not frequent enough. I thought I should be tested every week.  I did question the 2 week testing interval but I finally acquiesced to it because I trusted my team despite the fact that it just didn't seem like the prudent course. I will try very hard never to make that mistake again. I believed that I was too seasoned a patient to allow something like this to happen to me. And, I know that I am far more experienced than most patients and I cringe when I think of what other less experienced and less knowledgeable patients might permit and acquiesce to. It's a jungle out there and particularly so when you're sick.

Maybe ignorance is bliss in my case but I always do like to know what the real facts are - even if they aren't encouraging or favorable

Mike

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>my specialist works at the main pond
no matter how good you are, it's hard to be in two places at the same time. If you're seeing patients, you're not at the bench, no doubt part of the reason pathologists are so hard to reach. Next time you  see him, you might ask when was the last time he picked up a pipetman.

>make you stubborn as a mule
I suppose I should be grateful it's not a horse joke, but yes, I've already been warned in that regard... and thanks for the h pylori tip!
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Mike: He said "don't trust anyone" and I replied "except you, right?" and he said "no, not even me".
------------
Are you sure your surgeon isn't James Bond? Daniel Craig uttered similar to "M" at the end of "Casino Royal".
----------
Thanks for the detailed summary but curious why you would want a PCR of your biopsy tissue, esp in lieu of no other clinical problems.
]
If it's UND, that's great, but as DD will probably tell you , it still doesn't mean you are UND if  using ultra sensitive testing (in serum and/or tissue) that has been used only in studies, should you be in that camp.

And if it's positive, so then what? How would that alter treatment or your life? I doubt they would put you back on interferon if serum UND, unless you had other clinical issues. I personally see it as a lose-lose proposition until there is more understanding of what these things actually mean if they mean anything. Anyway, that's just my personal take, I'm sure you have your reasons.

-- Jim
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Willing: "...You might ask (your doc) was the last time he picked up a pipetman.
-------------------
But he's both married and straight. Maybe a pipetlady in his younger days.
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I figure that if they are going to take a tissue sample of my liver then they should test it for HCV. That seems so obvious to me I wonder whether I am understanding your question. I like to know as much as I can about me, my liver and HCV.
If your point is that there are more specific tests then the PCR that would probably be used I agree with that. But, if that is the threshold for testing why do we even get serum tests? We used them in the past when they were less sensitive than they are now and the current tests will likely not be as sensitive as they will be in the future. You use what you have. Mike
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My main point was what would you do with the info once you had it?

To my knowledge there are no tx protocols for people who are serum UND but liver tissue positive.

Personally, I would leave my SVR as SVR until someone showed me the clinical relevance of looking beyond, i.e. to leave well enough alone.  Not so much that "ignorance is bliss" but that more data without underlying clinical relevance doesn't really get you anywhere.

That said, I respect your desire to know "the real facts", and do let us know what you find out if and when the time comes.

-- Jim
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Let me take that back. In your very specific case -- liver transplant -- maybe the data could become useful in some very specific scenarios where a decision to use interferon again might come into play -- such as what happened last time. In other words, if they didn't find HCV in your tissue then it might make less sense to use interferon, but I'm way over my head in this area so please take this as speculation from someone that really doesn't understand the transplant and post transplant process.
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179856 tn?1333550962
Jim

I think it might be easier for you or I to let bygones be bygones but with someone who's been transplanted it might be a bit more of a pressing concern.  We haven't dealt with nearly the physical or mental aggravations and pain - personally if they were gonna be in my liver I'd feel like what the heck you might as well but if I'd been through the whole mess that he has...I'm pretty CERTAIN I'd want it done.
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Well Jim, I'm not running to get a biopsy so it's not an urgent matter. I am only saying that if I got another biopsy I would definitely insist that the tissue be tested for HCV. If you were to have a biopsy wouldn't you want the tissue tested? I think most of us would like to know as much as we can even if there isn't anything we can really do about it.
I want to know this stuff and what better place to learn than my own liver - particularly with my history. I would have thought my surgeon would have wanted to know for certain whether HCV was active in my liver. Looking back I think I was rejecting and it was as simple as that. Distinguishing acute rejection from HCV on biopsy is very difficult because they look the same. So how could the pathologist have known what was causing my inflammation and fibrosis? All the pathologist had before him was my age, my underlying disease and the date of my transplant. So he called it HCV. Perhaps if he had in front of him my serum undetectable tests since April of 2003 and my recent AR dose reduction he might have called it acute cellular rejection. I think that would have fit just as well as HCV.  
Basically we get a biopsy to learn about the state of our liver. A PCR of the tissue just adds to that information so it should have been done without question.
Mike
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Our posts probably crossed but that's pretty much what I said in my last post to Mike.
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As stated in probably what were crossed posts, I do agree with your decision and might do same in your shoes. But no, personally, I would not do it for myself for reasons originally stated nor in fact would I have another biopsy unless the docs felt my liver was acting up.
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Well we agree on that. I wouldn't have had a biopsy if I didn't have a problem. And that's why I won't run out and get one now. I don't mind them that much but it's not my favorite way to spend an afternoon either. And, you're right. Regardless of the results I cannot do anything about it. The point is I had the biopsy because my enzymes were elevating and I was also an SVR. Let's agree that a PCR of my tissue should have been done. If it ruled out HCV then it would have been far more likely that I was experiencing "some minor component of rejection" as the chief pathologist put it. And that would have been useful to know for many reasons not the least of which is to shed light on my chances to wean myself off of all the AR meds. Mike
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151263 tn?1243377877
Thanks for the clarification on the biopsy PCR results. I don't recall your entire history, I know it has many twists and turns though (this being one of them). One thing I was curious about though: Did you have HCV prior to your transplant and managed to SVR shortly thereafter? (via SOC) Or you did have HCV but managed to SVR just prior to your transplant? I can't remember what exactly happened. And the thing I'm wondering about, is that since people who have HCV (or test + for HCV antibodies) can and do donate livers upon their death - and considering that you would probably show up in the transplant recipient database as either having or had HCV, would that mean that you might (or would) get a liver from an HCV+ (or antibody +) person? Maybe you didn't and received a liver from a "clean" person never infected with HCV (SVR or otherwise). But considering the relatively close sequential timing of your treatment, SVR, and transplant combined with some possible bureaucratic chaos in how you may have been classified in the transplant database, I might be a bit concerned about the possibility of getting an infected liver, or perhaps a liver from an SVR which may have "persistent" virus in it.

But maybe not and you know for an absolute fact that your new liver was clean - just a thought I was curious about that may play into the whole confusion. I also wonder how new livers that become available for transplant are screened prior to transplant. Do they perfrom a PCR for HCV on them? Or simply measure for HCV antibodies? Or....???
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I was HCV positive prior to transplant. I was transplanted in June 2000 and I was diagnosed in January 1995 after a major variceal bleed.
I received an HCV negative liver. I saw that pathology report.
I treated within 2 months with regular interferon 3 x per week and low dose ribabvirin for 1 year. I didn't clear.
6 months after stopping my first treatment I retreated with standard dose Peg-Intron standard dose and low dose ribavirin for 53 weeks. I cleared late and relapsed immediately.
I treated a third time within 3 weeks of my second treatment. I treated for 73 weeks with standard dose Pegasys and weight based dose ribavirin. I cleared at week 12 or possibly week 11 and stopped in June 2004. I first tested undetectable in April 2003 and have never tested detectable since that time and I have tested every month since stopping in June 2004 with Heptimax <5 IU/ml.
I do not recall the particulars of the pathology report on my donor's liver. Since it was a cadaver liver I assume a PCR was performed on the tissue since no serum was probably available at my center. That is a good question though. I apologize for the fact that I will not investigate that issue. I've had enough of that stuff for a while.
Mike
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151263 tn?1243377877
"I apologize for the fact that I will not investigate that issue. I've had enough of that stuff for a while."

LOL Well I'd say you're off the hook, and I don't blame you for not bothering to check. But if (1) you've consistently tested serum UND with heptimax for more than 4 years running, especially (2) considering you've probably been taking immunosuppressants of one type or another during all this, and (3) you have teen-like enzymes, I'd say that should be good enough for just about anyone.

As another aside, I wonder if the donor liver or blood is tested using PCR? Normally I think of PCR results as having a rather long turn around time, and considering the shelf life and dispersion of donor livers (i.e. they may not all be located in a place where timely PCR testing can take place) it might not be feasible. Wouldn't surprise me if they simply check the donor's serum for HCV antibodies, and if + the liver is assumed to be HCV+. Especially considering the ongoing controversy about viral persistence anyway (similar to how HCV antibody positive people can't donate blood).
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As one who gets to ingest extremely powerful anti-rejection meds on a daily basis, I'd imagine that you (or anyone else in similar circumstances) and your docs would be very interested to know if low-level replication were taking place in your liver. For example, in the case of an occult+ liver PCR - the attending physician would most certainly want to know if there was a chance of the virus roaring back when making dosage level decisions and/or new or differing anti-rejection med choices. Undoubtedly there are other scenarios where this could be the case also: lagre doses of steroidals, etc.


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Tn,
my thoughts exactly.

mremeet,

Role of nucleic acid testing in cadaver organ donor screening: detection of hepatitis C virus RNA in seropositive and seronegative donors.
Aswad S, Khan NS, Comanor L, Chinchilla C, Corado L, Mone T, Mendez R, Mendez R.

National Institute of Transplantation; Los Angeles, CA, USA.

Hepatitis C virus (HCV) transmission by both seropositive and seronegative cadaver organ donors has been documented, yet nucleic acid testing is not routinely used to identify active infection in these donors prior to transplantation. Between November 2001 and February 2004, we screened 1445 cadaver organ donors for anti-HCV antibodies with either HCV EIA-2.0 (Abbott Diagnostics, Chicago, IL, USA) and/or Ortho HCV Version 3.0 ELISA (Ortho-Clinical Diagnostics, Raritan, NJ, USA) and confirmed seropositive samples with Chiron RIBA3.0 SIA (Chiron Corporation, Emeryville, CA, USA). Samples with sufficient volume (n = 726) were tested by the VERSANT HCV [transcription-mediated amplification (TMA)] Qualitative assay (Bayer Healthcare LLC, Tarrytown, NY, USA) which can be performed in approximately 5 h. Those with detectable HCV RNA and sufficient volume were quantified by the VERSANT HCV 3.0 (bDNA) Assay (Bayer Healthcare LLC) and/or the HCV RNA TMA Quantitative Assay (n = 23) and genotyped (n = 57). Seventy-seven of 1445 (5.3%) donors were seropositive, reactive by either one or both anti-HCV assays. Fifty-two of 63 (82.5%) of the seropositive samples had detectable HCV RNA and were genotyped. Seventeen of these samples had quantifications ranging from 128,123 to >7,692,307 IU/mL. Six of 663 (0.9%) seronegative samples had detectable HCV RNA. Their quantifications ranged from <9.3 to 1,464,799 IU/mL, and five of these six were successfully genotyped. As HCV RNA was demonstrated in samples from both our seropositive and seronegative cadaver organ donors, we are now incorporating nucleic acid testing into our donor screening/diagnostic algorithm.
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The above article alone is reason to be open to the concept of both 'occult' HCV as well as 'compartmentalized' HCV, both after SVR, in spontaneous resolvers, and maybe even in a portion of the population who have no apparent signs of HCV, such as antibody negatives, PCR negatives on serum testing, etc.  There are still riddles that are unsolved, and more to learn about HCV.  I continue to believe that the concept of either totally eradicated or 'infected', one or the other as our only descriptions, is both simplistic, given what we know, and is a limiting concept as far as future research.

DD
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I'm 3 yrs svr, doing great.  But, there's still the new new experiments where they are subjecting sero-neg, post inf, svr, immune cells to a "cocktail of mitogenic" stuff, and finding they are getting 100% of the subject samples to express some HCV RNA, and I think it's the neg-strand relicative stuff, and it's in the various immune cells, with different people having it in diff types of immune cells.  It seems that the reassuring stuff from Maylin, et al is not the same testing process, and suggests future immunocompromise or whatever cou;d wake the dragon.
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232778 tn?1217450711
Wow - talk about opening up an old and bitter (but enjoyable) thread...

I think Hep C is gone for good on SVR, but heck, what do I know? That's what I want to believe anyway, since I am SVR. To me, it is a totally academic question, because there is no real possiblity of relapse, so why bother studying or worrying about it?
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