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Replication of HCV in Liver AFTER SVR.
Here is the article cited today on HIV & Hepatitis website.
http://www.hivandhepatitis.com/hep_c/news/2007/121506_b.html
Most of us have seen this study, but seeing it highlighted on an international HCV related medical website sure draws some attention.
I wonder how all the HCV "cure" oriented doctors respond to this one? Here is the probable response: "Oh, its not an American study, must have shoddy standards." or, "The testing was probably not done properly"....OR..." Oooh...geez,I guess we were wrong, tx is really NOT a cure!!!!"...aaaa...well... maybe not the last comment!
http://www.hivandhepatitis.com/hep_c/news/2007/121506_b.html
Most of us have seen this study, but seeing it highlighted on an international HCV related medical website sure draws some attention.
I wonder how all the HCV "cure" oriented doctors respond to this one? Here is the probable response: "Oh, its not an American study, must have shoddy standards." or, "The testing was probably not done properly"....OR..." Oooh...geez,I guess we were wrong, tx is really NOT a cure!!!!"...aaaa...well... maybe not the last comment!
I am wondering why they didn't include people who naturally seroconverted?
Wouldn't you have?
I would have included them for this very reason. If this subgroup also has the same HCV remnants in the liver,PMBC then you can make generalized conclusions of the risks.
In Egypt alot of people have (or had) Hep C since the 1950's. You can look and see in those who naturally seroconverted had any increase in liver disease. If they didn't , then who cares.
Wouldn't you have?
I would have included them for this very reason. If this subgroup also has the same HCV remnants in the liver,PMBC then you can make generalized conclusions of the risks.
In Egypt alot of people have (or had) Hep C since the 1950's. You can look and see in those who naturally seroconverted had any increase in liver disease. If they didn't , then who cares.
Also lets say what above is true, that the virus is still replicating in the liver.
We can look at HBV as an analogy. When someone becomes an inactive carrier, the virus is usually undetectable in the blood. However we know that the virus is still replicating since we can detect the S antigen in the blood (S antigen is a by product of the HBV replicating).
So we have the same situation. The virus is not replicating so much it is detectable in the patients serum.
In the HBV case, studies show that no ongoing liver damage occurs. Progression to cirrhosis (outside other mitagating factors such as alcohol etc) is almost non existent. For HBV however there is a small risk since an intermediary molecule called cccDNA may have the ability to incorporate into the liver cells DNA and cause errors in copying and hence cancer.
HCV is an RNA molecule so I don't think this cancer risk is the same.
So we can conclude that even if its is the liver it is most likely doing no harm (as evident is improved liver histology from that study)
We can look at HBV as an analogy. When someone becomes an inactive carrier, the virus is usually undetectable in the blood. However we know that the virus is still replicating since we can detect the S antigen in the blood (S antigen is a by product of the HBV replicating).
So we have the same situation. The virus is not replicating so much it is detectable in the patients serum.
In the HBV case, studies show that no ongoing liver damage occurs. Progression to cirrhosis (outside other mitagating factors such as alcohol etc) is almost non existent. For HBV however there is a small risk since an intermediary molecule called cccDNA may have the ability to incorporate into the liver cells DNA and cause errors in copying and hence cancer.
HCV is an RNA molecule so I don't think this cancer risk is the same.
So we can conclude that even if its is the liver it is most likely doing no harm (as evident is improved liver histology from that study)
Nevertheless, liver damage ""improved"" in all but 2 patients.
Conclusion
"HCV persisted and replicated in the livers and peripheral blood mononuclear cells of ""MOST"" sustained responders," the authors concluded. "Thus, these patients did not experience HCV infection clearance, despite apparent clinical disease resolution
Conclusion
"HCV persisted and replicated in the livers and peripheral blood mononuclear cells of ""MOST"" sustained responders," the authors concluded. "Thus, these patients did not experience HCV infection clearance, despite apparent clinical disease resolution
I imagine the doctors you talk about would respond in the same way that they have been responding since as you state, this is not a new study.
Jensen, over at Clincial Options, puts it well where he basically calls SVR a cure in the clinical sense because patients that SVR show no detectible virus in serum in studies that run up to ten years and show improvement toward normal on follow-up liver biopsies, i.e. stoppage or regression of fibrosis/cirrhosis progression. My understanding is that he is not disputing the virologic presence in liver tissue of many SVR, but simply saying that there is no clinical significance, which I don't believe contradicts the study you cite. And to borrow a phrase from "Jboyhk" in his HBV analogy above, it appears that whatever virus is found in many (but not all) SVRs may be doing no harm.
-- Jim
Jensen, over at Clincial Options, puts it well where he basically calls SVR a cure in the clinical sense because patients that SVR show no detectible virus in serum in studies that run up to ten years and show improvement toward normal on follow-up liver biopsies, i.e. stoppage or regression of fibrosis/cirrhosis progression. My understanding is that he is not disputing the virologic presence in liver tissue of many SVR, but simply saying that there is no clinical significance, which I don't believe contradicts the study you cite. And to borrow a phrase from "Jboyhk" in his HBV analogy above, it appears that whatever virus is found in many (but not all) SVRs may be doing no harm.
-- Jim
Last sentence in my post above a bit confusing. Two points there. First point: not all SVRs show virus in liver tissue. Second point: In those that the virus is present, it may be doing no harm, unlike virus in serum which we know can do harm with progressively worsening liver histology and greater incidence of HCC.
A transplant perspective: Last Friday I saw my surgeon and though he got rushed to surgery we did have a few minutes.
He said that they have seen that transplant recipients who completely eradicate the virus are apt to have rejection issues. I asked him why and he said that apparently the virus has immunosuppressive properties.
He wasn't troubled at all by the HCV they found on biopsy - 30 IU/ml. He said I could live a long time with a little HCV (in light of the rejection issues maybe longer than if I was absolutely clear) if we can halt fibrosis and reduce my immunosuppressive dose to spare my renal function. I asked him why, after 2 years of TX, I would only show 30 IU/ml in my liver and he implied - he didn't come right out and state this unequivically - that there was a balance established whereby my immune system limited replication.
My personal opinion is that a small amount of HCV in the liver can and likely does cause very slow fibrotic activity - perhaps too slow, assuming no other factors are present eg..alcohol, fatty liver, drug toxicity etc. to result in any hepatic compromise or an increased susceptibility to developing HCC.
This is just my opinion and you guys know what that's worth - not much. Mike
He said that they have seen that transplant recipients who completely eradicate the virus are apt to have rejection issues. I asked him why and he said that apparently the virus has immunosuppressive properties.
He wasn't troubled at all by the HCV they found on biopsy - 30 IU/ml. He said I could live a long time with a little HCV (in light of the rejection issues maybe longer than if I was absolutely clear) if we can halt fibrosis and reduce my immunosuppressive dose to spare my renal function. I asked him why, after 2 years of TX, I would only show 30 IU/ml in my liver and he implied - he didn't come right out and state this unequivically - that there was a balance established whereby my immune system limited replication.
My personal opinion is that a small amount of HCV in the liver can and likely does cause very slow fibrotic activity - perhaps too slow, assuming no other factors are present eg..alcohol, fatty liver, drug toxicity etc. to result in any hepatic compromise or an increased susceptibility to developing HCC.
This is just my opinion and you guys know what that's worth - not much. Mike
I said "after 2 years <B>of</B> TX" but meant to say "after 2 years <B>off</B> TX".
That was misleading or otherwise I wouldn't have bothered to correct it. Mike
That was misleading or otherwise I wouldn't have bothered to correct it. Mike
I agree with everything said above, BUT, all I am trying to say is let's not just throw up our hands and cheer and think that the game is over! There MAY be clinical implications of this lingering virus, and if it is in the liver, have we yet determined where else it might 'persist'???
This is a line of research that bears LOTS more study, and eventually I think we all want CURE, with capital letters, rather than 'cure' with: ** see exceptions and exclusions in fine print below, side effects and ramifications may vary, etc.
I believe that the researchers are curious about what all this means, if not outright concerned about what it might involve. I do not want the medical community to just say, OK, we have the cure, do the treatment and you are just fine....if it turns out that there are ANY future medical or functional issues that might be attributed to the persistent virus.
I am not trying to be negative, or demean the SVR's that we have worked so hard to achieve...just to make sure that we are really in a good shape for the future as possible. We really do not know what the 'persistent virus' might do to us, or be doing to us right NOW. Are we sure that the immune system is not dys-regulated or hyper-activated due to the lingering virus? Are we sure that this lingering infection, which they do NOT describe as totally benign in the article, is not still causing some damage to the liver, or our immune system, but just at a much lower level?
If there are SOME people being tested who have NO signs of persistent virus after SVR, as the article describes, then wouldn't we ALL want to be able to have that outcome for ourselves? I sure would! If given a choice of lingering HCV, at sub-detectable levels in my liver and maybe other organs, and PBMC, lymphatic system, etc., OR, none whatsoever.....I know how I vote. Count me in for the NO HCV anywhere to be found.
On related issues: Do we really want the researchers to continue looking at HCV closely to see if it ends up in our brain, our CNS, connective tissues, etc. and what effects that is having on us....both before tx, AND after SVR?
Or do we just want to go into a sort of denial, and say, I'm just fine....totally cured you know....not to worry....
I think we need to find out lots more, and we will anyway whether we want to or not. There may be reasons for all the post-tx symptoms that don't JUST relate to all the interferon that we did. How about the people who SVR and have continued longterm disabling fatigue. My doctor says there is a large group with this outcome...close to 50% possibly.
I think we want more answers. I'm not ready to close the book just yet.
DoubleDose
This is a line of research that bears LOTS more study, and eventually I think we all want CURE, with capital letters, rather than 'cure' with: ** see exceptions and exclusions in fine print below, side effects and ramifications may vary, etc.
I believe that the researchers are curious about what all this means, if not outright concerned about what it might involve. I do not want the medical community to just say, OK, we have the cure, do the treatment and you are just fine....if it turns out that there are ANY future medical or functional issues that might be attributed to the persistent virus.
I am not trying to be negative, or demean the SVR's that we have worked so hard to achieve...just to make sure that we are really in a good shape for the future as possible. We really do not know what the 'persistent virus' might do to us, or be doing to us right NOW. Are we sure that the immune system is not dys-regulated or hyper-activated due to the lingering virus? Are we sure that this lingering infection, which they do NOT describe as totally benign in the article, is not still causing some damage to the liver, or our immune system, but just at a much lower level?
If there are SOME people being tested who have NO signs of persistent virus after SVR, as the article describes, then wouldn't we ALL want to be able to have that outcome for ourselves? I sure would! If given a choice of lingering HCV, at sub-detectable levels in my liver and maybe other organs, and PBMC, lymphatic system, etc., OR, none whatsoever.....I know how I vote. Count me in for the NO HCV anywhere to be found.
On related issues: Do we really want the researchers to continue looking at HCV closely to see if it ends up in our brain, our CNS, connective tissues, etc. and what effects that is having on us....both before tx, AND after SVR?
Or do we just want to go into a sort of denial, and say, I'm just fine....totally cured you know....not to worry....
I think we need to find out lots more, and we will anyway whether we want to or not. There may be reasons for all the post-tx symptoms that don't JUST relate to all the interferon that we did. How about the people who SVR and have continued longterm disabling fatigue. My doctor says there is a large group with this outcome...close to 50% possibly.
I think we want more answers. I'm not ready to close the book just yet.
DoubleDose
I agree it deserves more study but honestly, I don't care if they spend one thin dime researching this UNTIL they find us a solution that works for all with HCV. I wish they would focus the funding available on knocking this virus out for all. How about the nonresponders or those who cant take IFN?? I worry about them before I worry about people who cleared this virus who have ongoing but MILD symptoms. the amounts they find are so small they have to really look hard even to find it.
Put the research dollars there, get people across the board SVR, then if we have some errant small amount of virus hanging around in all the SVR'ed people, they can spend the funds looking into it but people won't be DYING from it!
Comparatively speaking, these mild symptoms seem insignificant to me when there are people with HCV still attacking them and destroying their livers, causing other diseases, etc.
This small amount they are finding in SVR's they conclude is NOT causing liver damage.
Put the research dollars there, get people across the board SVR, then if we have some errant small amount of virus hanging around in all the SVR'ed people, they can spend the funds looking into it but people won't be DYING from it!
Comparatively speaking, these mild symptoms seem insignificant to me when there are people with HCV still attacking them and destroying their livers, causing other diseases, etc.
This small amount they are finding in SVR's they conclude is NOT causing liver damage.
DD:
1)If there are SOME people being tested who have NO signs of persistent virus after SVR, as the article describes, then wouldn't we ALL want to be able to have that outcome for ourselves?
2)On related issues: Do we really want the researchers to continue looking at HCV closely to see if it ends up in our brain, our CNS, connective tissues, etc. and what effects that is having on us....both before tx, AND after SVR?
Or do we just want to go into a sort of denial, and say, I'm just fine....totally cured you know....not to worry....
---------------
Regarding #1 -- only if there is a clinical benefit. If not clinical, i.e. doing "no harm", then what's the point of risking further treatment? And, as Mike suggests, there may even be a benefit for some. Not cut and dry at all to me.
Regarding #2 -- don't think anyone is saying research should stop in this important area. Just saying let's not jump to conclusions before there are any. Someone mentioned recently that I believe their doctor told them that if you looked "hard enough" at someone cured from cancer you'd still find something -- but again, that doesn't mean this person *has cancer*. Most of us carry some sort of markers from different viruses like Epstein Barr, etc, but it appears to do no damage in those with a healthy immune system.
1)If there are SOME people being tested who have NO signs of persistent virus after SVR, as the article describes, then wouldn't we ALL want to be able to have that outcome for ourselves?
2)On related issues: Do we really want the researchers to continue looking at HCV closely to see if it ends up in our brain, our CNS, connective tissues, etc. and what effects that is having on us....both before tx, AND after SVR?
Or do we just want to go into a sort of denial, and say, I'm just fine....totally cured you know....not to worry....
---------------
Regarding #1 -- only if there is a clinical benefit. If not clinical, i.e. doing "no harm", then what's the point of risking further treatment? And, as Mike suggests, there may even be a benefit for some. Not cut and dry at all to me.
Regarding #2 -- don't think anyone is saying research should stop in this important area. Just saying let's not jump to conclusions before there are any. Someone mentioned recently that I believe their doctor told them that if you looked "hard enough" at someone cured from cancer you'd still find something -- but again, that doesn't mean this person *has cancer*. Most of us carry some sort of markers from different viruses like Epstein Barr, etc, but it appears to do no damage in those with a healthy immune system.
DD: How about the people who SVR and have continued longterm disabling fatigue. My doctor says there is a large group with this outcome...close to 50% possibly.
----------------------------------
I've had bouts of fatigue prior to treating and it certainly would have been nice if it disappeared after SVR, which it did not. But to blame the fatigue on HCV is pure speculation, as fatigue is one of the most common complaints every doctor hears from all patients, whether or not they have HCV. I have a relative who has had chronic fatigue for most of their life and they do not have HCV. And no, it wasn't some sort of occult familial transmission because their fatigue pre-dates my infection. Ask ten of your non-HCV friends if they are fatigued a lot and I'll bet five say "yes". So there's your 50%. My personal thoughts are that the kind of fatigue many of experience are due to the stress of modern living combined with a high-fat diet, and frequently not enough prolonged exercise.
-- Jim
----------------------------------
I've had bouts of fatigue prior to treating and it certainly would have been nice if it disappeared after SVR, which it did not. But to blame the fatigue on HCV is pure speculation, as fatigue is one of the most common complaints every doctor hears from all patients, whether or not they have HCV. I have a relative who has had chronic fatigue for most of their life and they do not have HCV. And no, it wasn't some sort of occult familial transmission because their fatigue pre-dates my infection. Ask ten of your non-HCV friends if they are fatigued a lot and I'll bet five say "yes". So there's your 50%. My personal thoughts are that the kind of fatigue many of experience are due to the stress of modern living combined with a high-fat diet, and frequently not enough prolonged exercise.
-- Jim
2 months post-trx and i have fatigue,joint pain and stamina issues..these are much more pro-nounced than pre-trx..Is this just interferon 'hang-over' or ongoing residual hep manifested sx's??...Addled minds need to know!..I do indeed want a SVR =CURE..
Recently I was sitting in the waiting room of my drug trial clinic awaiting my appointment with our study nurse. This clinic treats HIV and/or HCV infected people and performs extensive research on new drugs (like VX950). They had a 'clinic circular' mini-newspaper in their magazine rack that I was reading, and it discussed the phenomenon of HIV persistence (something I know zero about). Apparently HIV infects your "CD4" immune cells and once there, can remain sheltered and unscathed in a dormant state for up to 70 years. The CD4 cells are incredibly long lived within our bodies, and that's why HIV cannot be currently cured. Even in the presence of powerful and very effective HIV antiviral cocktails that cleanse the blood of almost all HIV (and keep these patients alive and healthy), there are always at least a few entrenched HIV virii that will 'hold out' within some of the patient's very long lived CD4 cells. This apparently is the primary reason why HIV cannot be cured today, and can only be treated/controlled as an ongoing chronic illness.
The article went on to explain that there is currently ongoing research looking into finding a way to get rid of these long lived infected CD4 cells. They were describing possible treatment strategies in the future where they might be able to chemically identify infected CD4 cells and then provoke them to die and disgorge their infective contents. Once exposed and removed from the shelter of the CD4 cell, the virus can then be destroyed via the current antiviral drugs. If this can be achieved, then it's thought HIV can actually and truly be *cured*.
When I read that article it made me think of the current low level 'viral persistence' theory for SVR-ed HCV patients. If it turns out the low level HCV infection is true, and it's also clinically significant (i.e. it poses some risk/harm to the patient), then I can see where a similar strategy may be employed in the future to route out the remaining vestiges. A drug or gene therapy that can somehow identify HCV infected cells within the body and trigger them to die in order to dislodge the last remnants of the HCV holdouts. If powerful antiviral drugs were being taken simultaneously, then this could finally rid ourselves of the bugs once and for all.
Lastly, I think it's also important to remember that not only does achieving an SVR status provide very substantial health benefits for at least 10-15 years, it builds a bridge to the future. It stops the damage to your liver and usually allows for at least some healing and reversion of existing fibrosis. And this benefit is durable for at least a decade and almost certainly much longer. But even if the durability of an SVR status does have an expiration date (say 20 years into the future), what will be the status of HCV research that far into the future? I think it's pretty clear at this point that within ten years there will be much more effective, shorter and more humane treatments for HCV - possibly including some that can eliminate any low level persistent virus. And the effectiveness of the drugs will only get better the further into the future we go. Plus they're currently working on anti-fibrotics which will in all likelihood be developed and accessible within 10-20 years. So even if the SVR status has a drop dead date of 10 or 20 years, it can still serve as a sort of lifesaving "time machine" that can transport you and your liver (intact) to a time and place into the future where there will be a true cure. (not unlike the how cryogenics is viewed today...by some, anyway ;-)
The article went on to explain that there is currently ongoing research looking into finding a way to get rid of these long lived infected CD4 cells. They were describing possible treatment strategies in the future where they might be able to chemically identify infected CD4 cells and then provoke them to die and disgorge their infective contents. Once exposed and removed from the shelter of the CD4 cell, the virus can then be destroyed via the current antiviral drugs. If this can be achieved, then it's thought HIV can actually and truly be *cured*.
When I read that article it made me think of the current low level 'viral persistence' theory for SVR-ed HCV patients. If it turns out the low level HCV infection is true, and it's also clinically significant (i.e. it poses some risk/harm to the patient), then I can see where a similar strategy may be employed in the future to route out the remaining vestiges. A drug or gene therapy that can somehow identify HCV infected cells within the body and trigger them to die in order to dislodge the last remnants of the HCV holdouts. If powerful antiviral drugs were being taken simultaneously, then this could finally rid ourselves of the bugs once and for all.
Lastly, I think it's also important to remember that not only does achieving an SVR status provide very substantial health benefits for at least 10-15 years, it builds a bridge to the future. It stops the damage to your liver and usually allows for at least some healing and reversion of existing fibrosis. And this benefit is durable for at least a decade and almost certainly much longer. But even if the durability of an SVR status does have an expiration date (say 20 years into the future), what will be the status of HCV research that far into the future? I think it's pretty clear at this point that within ten years there will be much more effective, shorter and more humane treatments for HCV - possibly including some that can eliminate any low level persistent virus. And the effectiveness of the drugs will only get better the further into the future we go. Plus they're currently working on anti-fibrotics which will in all likelihood be developed and accessible within 10-20 years. So even if the SVR status has a drop dead date of 10 or 20 years, it can still serve as a sort of lifesaving "time machine" that can transport you and your liver (intact) to a time and place into the future where there will be a true cure. (not unlike the how cryogenics is viewed today...by some, anyway ;-)
I want to be clear that I am not trying to make my personal situation central to this discussion but there might be some application to the general HCV community.
I have shown only 30 IU/ml on biopsy and yet been serum undetectable monthly for 2.5 years off TX.
We know the virus can replicate at 10 to the twelfth power so my HCV is obviously not replicating as successfully as it could be and formerly was.
My sugeon said that transplant patients who have completely eradicated all trace of HCV have been more prone to organ rejection issues.
Is is not reasonable or possible to deduce that the little bit of HCV which remains or persists in me requires my immune system to keep it in check and thereby exerts an immunosuppressive influence which may help to insulate me from rejection?
If this is true, wouldn't it possibly suggest that in those non-transplant SVRs who still have a bit of persistent HCV that their immune system would need to also spend some resources keeping the HCV in check? Now what this means to overall immune system vitality I haven't a clue but it seems like this is something to think about.
Mike
I have shown only 30 IU/ml on biopsy and yet been serum undetectable monthly for 2.5 years off TX.
We know the virus can replicate at 10 to the twelfth power so my HCV is obviously not replicating as successfully as it could be and formerly was.
My sugeon said that transplant patients who have completely eradicated all trace of HCV have been more prone to organ rejection issues.
Is is not reasonable or possible to deduce that the little bit of HCV which remains or persists in me requires my immune system to keep it in check and thereby exerts an immunosuppressive influence which may help to insulate me from rejection?
If this is true, wouldn't it possibly suggest that in those non-transplant SVRs who still have a bit of persistent HCV that their immune system would need to also spend some resources keeping the HCV in check? Now what this means to overall immune system vitality I haven't a clue but it seems like this is something to think about.
Mike
As long as we're speculating -- along the lines of your discussion, I suppose one could deduce that we're blessed to have "persistent" virus in us as it may be giving us a superhuman immune system> Next thing we're going to read is that SVRs live ten years longer than the general (non HCV) population. You know the Nietzsche principle of HCV -- if all the virus isn't killed, it makes us stronger :)
Be well,
-- Jim
Be well,
-- Jim
ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer ten years longer
SVR already does that, they don't have the virus still attacking them. I do think it needs investigation but since it doesnt appear to be making people sick even if it is found it is less important that finding a solution that can at least get all with HCV so it isnt detectable in their serum.
Im sure you can find remants or evidence of lots of viruses we have been expoed to or had in our lifetimes but they aren't hurting us and as Mike points out could even help us in those miniscule amounts.
Im sure you can find remants or evidence of lots of viruses we have been expoed to or had in our lifetimes but they aren't hurting us and as Mike points out could even help us in those miniscule amounts.
Again, you have given the discussion your own personal interpretation. These were not described as remnants, but actual long term replicating HCV virus. both positive and negative strand. No one has said that there are no clinical implications over the long haul, this is exactly what the researchers are now studying. Also, as Mike suggested, all this immune system stimulation MAY cause problems for us, and at least deserves study. If the virus is being held in-check by our immune systems, then this is a whole different scenario than harmless remnants, and it does not equal CURE, but remission, which is now the term being used by many doctors, and HCV organizations. I do not believe that the medical establishment has said that this persistent virus is harmless, and in fact the article suggested ongoing necro-inflammatory activity in the liver, at a lower level than previous to SVR. So, yes our livers improve, but are still infected, and still experiencing low level damage, and also MAY be much more susceptible to HCC or other problems over ten or twenty years.
There is no reason in the world why they should not simultaneously explore all these important issues while treating people with the current tx technology. Just because you say it will not cause problems for us, does not mean that there is any factual or scientific basis for your judgement. And that is just why they continue to do study after study to understand this phenomenon. The studies will increase in number, and complexity. Better treatments will eventually emerge as a result of this line of study, as was suggested above in the case of HIV and future CURE oriented treatments.
DoubleDose
There is no reason in the world why they should not simultaneously explore all these important issues while treating people with the current tx technology. Just because you say it will not cause problems for us, does not mean that there is any factual or scientific basis for your judgement. And that is just why they continue to do study after study to understand this phenomenon. The studies will increase in number, and complexity. Better treatments will eventually emerge as a result of this line of study, as was suggested above in the case of HIV and future CURE oriented treatments.
DoubleDose
I don't see anyone saying they shouldn't study it. Never have I seen anyone say it doesn't need more study actually. I do not believe those remants or particles or persistent or whatever you call them, are causing most people anything because that is what all these studies have said, no symptoms no nothing at ALL except they can find it in small amounts,but not in your serum.
Im all for them studying it once we solve the main issue, getting people so their bodies aren't being virally attacked. What to do with any residuals (that aren't hurting you)and what it will mean and how many people have it is yet to be determined.
Although irritating and difficult to cope with, the symptoms you describe are not threatening your life.
To me there is no debate, ALL things HCV need to be studied I just think my priorities are on SVR for all. The left over viral stuff, all we have are these few small papers on it. It is very much under debate. You speak of it as if it's a foregone conclusion at times.
Im all for them studying it once we solve the main issue, getting people so their bodies aren't being virally attacked. What to do with any residuals (that aren't hurting you)and what it will mean and how many people have it is yet to be determined.
Although irritating and difficult to cope with, the symptoms you describe are not threatening your life.
To me there is no debate, ALL things HCV need to be studied I just think my priorities are on SVR for all. The left over viral stuff, all we have are these few small papers on it. It is very much under debate. You speak of it as if it's a foregone conclusion at times.
I think we all agree that:
A)SVR is the primary goal and absolutely confers tremendous benefits 1)halts or drastically slows down fibrosis and 2)dramatically reduces the likelihood of developing HCC.
B)In some SVRs HCV can and does persist and it some it appears as though the virus is 100% eliminated.
C)More research is needed to ascertain what,if any, long term consequences can result from low level persistent HCV and what can be done to eliminate all traces of the virus and/or prevent any damage from occurring as a result of it.
Is that safe to say?
The rest, for the most part, is theoretical and academic and I'm all for theorizing but we should always keep in mind the points of aggreement.
Mike
A)SVR is the primary goal and absolutely confers tremendous benefits 1)halts or drastically slows down fibrosis and 2)dramatically reduces the likelihood of developing HCC.
B)In some SVRs HCV can and does persist and it some it appears as though the virus is 100% eliminated.
C)More research is needed to ascertain what,if any, long term consequences can result from low level persistent HCV and what can be done to eliminate all traces of the virus and/or prevent any damage from occurring as a result of it.
Is that safe to say?
The rest, for the most part, is theoretical and academic and I'm all for theorizing but we should always keep in mind the points of aggreement.
Mike
You said it succinctly. That's all that needs to be said.
DD
DD
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