HR: Therefore there is no pattern or specific reason that we can pinpoint beyond speculation why all of the sudden your exercise did not cause these flares anymore.
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I guess you're confirming what I very strongly suspected, that intense exercise way back then brought the virus back (high enzymes, jaundice, etc) even though they had no way of directly measuring it then. Perhaps had I taken it easier, my immune system would have cleared the virus on its own.
But then it stopped happening for some reason, with the one exception of my flair (ALT over 600) four years ago during the week I took the hep b booster, and Chinese herbs, I also had a couple of intense workouts. But that's just speculation.
Of course, my concern is the present. Do you think at this point -- SVR and 9 months post EOT -- that I should be concerned at all about intense exercise? I posed this question to my hepatologist and he said "no" but I would like your take.
-- Jim
See, told you exercise was bad. HR and I are hitting the bar for some weight based cheesburges and Peg fries - game is gonna start soon! Seriously, though my theory is this - and its just a theory, it could be self serving bullsh!t for all I know - that with no virus (maybe) and a better liver (definitely) that I will proceed to better health naturally and that my weight will follow. More energy, more optimism, more activity, less weight etc. Make sense? I assume that this may require me to stop feeding my face and get my arse off the couch one of these days but right now magical thinking is good enough for me.
Vigorous exercise can be quite an immunesupressant. I have seen swimmers whose HBV broke into flares after intense training.
Each of your flares was followed by a slight change in the virus quasispecies that "swarmed" invisibly inside you after the flare, because new epitopes were created, new viral fitness was obtained and so much more. Therefore there is no pattern or specific reason that we can pinpoint beyond speculation why all of the sudden your exercise did not cause these flares anymore.
the lack of improvement typical afterr tx:
I formulated the possibilities as questions to indicate that those are alternative or parallel possibilities that only very expensive and extensive research can start to answer. I say extensive, since Vincente Carrenos results are ignored by many clinicians, unless confirmed in several large series. Plus, the question re the potential fitness of these residuals was not even remotely addressed.
2. Is the maintainance of this response - to a dramatically varying degree in various individuals - still a constant unspecific immune stimulans, responsible...
for some or many or most of the "after tx syndromes" that DD and others are suffering from?
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1) From what I've read and experienced, the majority of "after tx syndromes" that DD and others discuss may be as easily attributable to the interferon tx itself as opposed to any unspecific immune response. I say this because in many cases, the symptons discussed were not present before treating and only present after treating. So, unless, the post-tx response to the viral remants is more agressive than the pre-tx response to the whole virus -- at least to me it suggests the cause of these symptons is from an interferon-altered immune system and not from the virus.
2) Related, very few report "feeling better" after treatment. With some exceptions, most report about the same and many feeling worse such as DD. In my case, I'm starting to get very close to feeling the way I did pre-tx but I can't say I feel any better, stronger, etc. This seems to argue for the point of view that HCV is in many, if not most cases, totally asymptomatic (no extrahepatic stuff) until a higher level of cirrhosis takes place.
Otherwise, why wouldn't a number of us SVRs report a dramatic improvement in how we feel? Or, is it the virus in 'other' compartments that prevents us from feeling dramatically better?
On a personal note, I led a very active life since contracting hep c around 1970, at times succesfully competing in endurance events with men much younger. Still, I had periods of fatigue during training that I thought were attributable to the virus. But now the virus is gone, and again, I feel about the same. Of course, I'm very happy I no longer have the virus and that my liver histology seems to be improving. But where I come out is maybe that is all that one can expect from treatment -- improved liver histology and perhaps less chance of HCC. Many of those pre-tx seem to think that a lot of their 'symptons' will disappear once they SVR. Afraid there will be lots of disappointments.
Interested in your take on both #1 and #2. Thanks again.
--Jim
I had an acute stage of HCV around 1970. Enzymes over 1000 if I remember correctly with jaundice, dark urine, white stools, etc. Over the next 4 years I had 2-3 acute relapses. Each relapse was associated with a significant increase in physical activities such as running. Then all of a sudden I went into a "hold" pattern where physical activity didn't seem to have any effect on the virus and therefore the enzymes remained more or less consistently mildly elevated until I started treating. They did go into the high-normal range however, whenever I went on a strict low fat diet such as Pritikin which is total fat calories less than ten per cent of total calories. But because of my past history, always a little anxiety if I start feeling sluggish after some hard work outs. Intellectualy, I understand that exercise won't bring the virus back but it apparently did cause relapse way back then. I guess that's why I took my recent enzymes and viral load tests at 9 months post tx. Since my ALT is 15 I guess nothing to worry about. Still, curious on your take about vigorous exercise and my early acute relapses and why all of a sudden it became a non issue. Discussed this with a couple of well-known hepatologists in the early 70's and they said that the exercise could have brought on the relapses but it was just speculation.
Thanks again for all your help.
-- Jim
Jim wrote
I believe what HR stated -- and sure I'll be corrected if wrong -- however, is that if many of us were tested frequently *after* SVR with very sensitive tests (like Heptimax) that every once in a while we might find ourselves with a low level of virus.
My point was that if this were true, wouldn't we see more postive viral loads after SVR since tens of thousands of people are being tested post SVR and yet we don't see those positive results except in rare cases. So in essence, this theory has been tested -- perhaps not on an individual patient, but on a mass grouping which might substitute.
Response
The theory has not really been tested, the diluted "raw data" are scattered among many labs, drs, patients....If someone publishes re the stability of SVR, he will not refer to spurious, not confirmable positives.
There is actually now little question that "some" might test positive "occasionally" with positive tests after SVR. How frequently however is simply a question of how low the average remaining VL - and i said average, because it could be zero in some - is. At one copy/ml - below the official detection limit of all commercial tests- there are still approx ten thousand virions circulating. If you had ten only circulating you would then need at least one thousand tests to catch one on the average...
Again all that really matters is the tested mean stability of SVR.
But there are important questions beyond that that DD is constantly referring to.If remnant virus does stay around in some compartments,
1. Is it genetically altered, dramatically less fit but still maintains some critical Tcell or B cell epitopes to be effectively recognized by the incredibly sensitive and powerful CD8T cell response?
2. Is the maintainance of this response - to a dramatically varying degree in various individuals - still a constant unspecific immune stimulans, responsible
a. by itself
b. in connection with the imprinted overdrive of immune responssiveness imprinted by IFN TX
for some or many or most of the "after tx syndromes" that DD and others are suffering from?
3. Is the across the board genetic shift of the remnants - IFN survivors after all- the major reason for the stability of SVR? I call this "lateral evolution" of HCV to a much more benign, tamed, ultra low copy molecular parasite or is
4. the heigtened T helper cell surveillance the key aspect of SVR stability or
5. an improved B cell blockage of small remnants the key to blockage of "internal reinfection" or spread? ( In case you have not heard there is not just HBIG but also HCIG investigated, as reinfection blocker after transplant, with very limited success however)
6.Simply not a single intact virion anywhere in the body that could become the great grandfather of a new spread. Gone,CURED. Ready for external reinfection maybe, but not from the inside, regardless of chemotherapy, antirheumatics, TNFalpha blockers, ANAKINRA and so on....
A small note re the presence of the virus in the lymphatic system: Viruses often enter this system, because it is supposed to pick them up, process them, present them etc. That system typically does not get attacked for the presence of the virus ( HIv a big exception), for obvious reasons. Viruses do also not normally thrive inside this system, so it is not a big problem, but it can become a reservoir.
Jim, your AST/ALT ratio is fine in that low absolute range of AST. If in the high range it would be a sign for cirrhosis as a quick search in Pubmed will convince you. Your workouts will increase the AST also somewhat. As a matter of fact, your ALT as well to a lesser degree, so I suspect you dont even work out that hard yet to have a 15 ALT.