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HepC positive after 48 weeks of Treatment
I did a full 48 weeks of 2b-pegintron combo therapy and 2 months after treatment I got sick and the virus is now elevated. At the half way mark I was undetectable. Now I have to go in every month to keep track of my ALTs. The Doc says that there is no other treatment now that can help and all I can do right now is hope for a new treatment and try to stay healthy. They seemed concerned at the virus count. I know there is no correlation between high count and liver damage but its same old ****. Tired all the time, headaches and the Lichen Planus is flaring up again. At first I thought it was my body adjusting to being off treatment, at least hoping but I was wrong.
A couple of questions. Can the virus cross the blood/brain barrier? Can the treatment cross the barrier? Could this be the reason that others and me can
A couple of questions. Can the virus cross the blood/brain barrier? Can the treatment cross the barrier? Could this be the reason that others and me can
thanks for all the info. Indiana if you could post the cite that recommended keeping riba doses as high as possible I'd be very interested to read more about it. My Dr. was unwilling to increase my dose from 1000 to (weight-approoriate) 1200 and since I *really* dislike the stuff (more for its mutagenic behavior that its sides) I've been happy to comply - but maybe I should be investigating further.
Looks like at present 1's can expect about a 30% relapse rate (<a href="http://www.hivandhepatitis.com/2003icr/38easl/docs/032103b.html">
relapse stats </a>) whereas the studies reporting presence and replication of hcv in the cns all found higher percentages (8/13, 3/6, 6/6). So even if you have hcv actively replicating in your brain (and it looks like many of us do) combo therapy can successfuly clear it. (btw another paper by the same authors in Mike's cite is <a href="http://jvi.asm.org/cgi/content/full/76/19/10064"> here </a>
This inclination of sequence-specific strains to specialize in different cell-types (serum, cns, lymph, liver) is pretty interesting. Kind of argues for drugs that go after a "common denominator" aspects of the virus.
Looks like at present 1's can expect about a 30% relapse rate (<a href="http://www.hivandhepatitis.com/2003icr/38easl/docs/032103b.html">
relapse stats </a>) whereas the studies reporting presence and replication of hcv in the cns all found higher percentages (8/13, 3/6, 6/6). So even if you have hcv actively replicating in your brain (and it looks like many of us do) combo therapy can successfuly clear it. (btw another paper by the same authors in Mike's cite is <a href="http://jvi.asm.org/cgi/content/full/76/19/10064"> here </a>
This inclination of sequence-specific strains to specialize in different cell-types (serum, cns, lymph, liver) is pretty interesting. Kind of argues for drugs that go after a "common denominator" aspects of the virus.
Thanks for this great discussion everyone. My symptoms started in February of this year with numbness in my hands, feet, arms and legs. The docs first tested for thyroid, then a couple of MRI's, and lots of blood work. When I was diagnosed with HCV, the neurologist wanted me to treat it first before we do any additional cns testing. So, I am doing shot #10 tomorrow (of 24) and will be curious to see if I clear the hepatitis if my neuro problems will go away. Thanks again - Cheryl
What a WAY cool thread.
Hey MCN...I'm really sad to hear that you're feeling bad. I hope they can figure something out for you.
I have been reading up a bit on some of this blood/brain stuff. Sorry Bunkywoo, but they're usin cadavers for these findings of brain damage levels. It does seem that the virus can cross that barrier and once there can cause some damage. It doesn't happen to everyone. The interferon cannot cross the barrier. Neither can many other drugs like penicillin. But some other drugs CAN....like erythromycin. They speculate that the Riba can have some good effects across the barrier. That is why they seem to find an improvement in brain function in those who undergo tx. The spinal fluid is totally replaced about 3 times a day so that is not where the problem is. The brain fluid is only replaced at a rate of about 30% a year, so anything in there is a problem. They speculate that keeping the Riba doses as high as possible does help wiht slowing or preventing replication in the brain. Since the virus does have a life limit if it can be prevented from replicating then it will die on its own. More good news is that the protease inhibitors DO work across this barrier which makes their approval for treating this stuff even more exciting.
Before we all freak out over this discussion let me say that these findings are not all that new. And they do NOT affect the overall success rates of those doing tx. This whole thing is good only to explain ONE of the possible reasons why some people succeed and some don't. It does NOT account for the "brain fog" that most of us get during tx. Having "brain fog" does NOT mean that you have Hcv in your brain. Many other things can account for that like ammonia levels, anemia, etc. Just don't let this freak you out.
Overall, the song remains the same. Do your meds. Do your best to adhere to the dosing schedule. Try to keep your anemia at bay so as to stay on the highest doses possible of the meds. Go for as long as you can on the tx. Then cross your fingers and hope for the best. MOST of us will succeed at this overall. MOST of us will NOT have any lasting side effects. Even most of those who don't remain clear will have helped their condition. The positives still outweigh the negatives here.
So keep those hopes HIGH! STAY POSITIVE!! Depression is our enemy! Do your meds, wear your hat,slather on your skin coatings, put on your WAY cool shades, and go outside and kill something. Whatever it takes to make you feel better. Keep moving forward and never look back. This Dragon just HATES us when we are happy, positive, and persistant.
Keep the faith...........................
Hey MCN...I'm really sad to hear that you're feeling bad. I hope they can figure something out for you.
I have been reading up a bit on some of this blood/brain stuff. Sorry Bunkywoo, but they're usin cadavers for these findings of brain damage levels. It does seem that the virus can cross that barrier and once there can cause some damage. It doesn't happen to everyone. The interferon cannot cross the barrier. Neither can many other drugs like penicillin. But some other drugs CAN....like erythromycin. They speculate that the Riba can have some good effects across the barrier. That is why they seem to find an improvement in brain function in those who undergo tx. The spinal fluid is totally replaced about 3 times a day so that is not where the problem is. The brain fluid is only replaced at a rate of about 30% a year, so anything in there is a problem. They speculate that keeping the Riba doses as high as possible does help wiht slowing or preventing replication in the brain. Since the virus does have a life limit if it can be prevented from replicating then it will die on its own. More good news is that the protease inhibitors DO work across this barrier which makes their approval for treating this stuff even more exciting.
Before we all freak out over this discussion let me say that these findings are not all that new. And they do NOT affect the overall success rates of those doing tx. This whole thing is good only to explain ONE of the possible reasons why some people succeed and some don't. It does NOT account for the "brain fog" that most of us get during tx. Having "brain fog" does NOT mean that you have Hcv in your brain. Many other things can account for that like ammonia levels, anemia, etc. Just don't let this freak you out.
Overall, the song remains the same. Do your meds. Do your best to adhere to the dosing schedule. Try to keep your anemia at bay so as to stay on the highest doses possible of the meds. Go for as long as you can on the tx. Then cross your fingers and hope for the best. MOST of us will succeed at this overall. MOST of us will NOT have any lasting side effects. Even most of those who don't remain clear will have helped their condition. The positives still outweigh the negatives here.
So keep those hopes HIGH! STAY POSITIVE!! Depression is our enemy! Do your meds, wear your hat,slather on your skin coatings, put on your WAY cool shades, and go outside and kill something. Whatever it takes to make you feel better. Keep moving forward and never look back. This Dragon just HATES us when we are happy, positive, and persistant.
Keep the faith...........................
I've been studying this brain issue and I may be way over my head. I also may be learning stuff that will depress me a little. The good news for you guys is that the association with HIV is probably explained by the immune deficiency. Quoting the text: http://jvi.asm.org/cgi/content/full/76/2/600?ijkey=3f374694848d38403d93ab9f2bae7da265c974a9
An important question is that of how the HCV got into the CNS. In theory, HCV could gain access to the brain by way of cerebrospinal fluid as occurs in visna virus infection (12). Alternatively, and more likely, neuroinvasion is related to trafficking of infected cells of monocyte/macrophage lineage through the blood-brain barrier, in a process similar to that postulated for HIV-1 infection (28, 35). Subsequently, there could be a secondary spread of HCV to permissive resident microglial cells within the brain. Replication in the CNS could be facilitated by immunosuppression, some degree of which was likely to be present in all of our patients. This possibility is supported by the observations that while HCV negative-strand RNA is rarely detected in PBMC from normal subjects (15, 24), it is commonly found in HIV-coinfected patients or liver transplant recipients (16, 30). Moreover, HCV replication was demonstrated in hematopoietic cells inoculated into severe combined immunodeficiency mice (5). However, HCV replication in bone marrow was also found in some obviously immunocompetent subjects (29, 31).
The observed concomitant infection of the same host by two different HCV strains, each replicating in a different compartment, is probably the consequence of coinfection or superinfection with strains manifesting different tropisms for different cells. For example, it has been demonstrated for lymphocytic choriomeningitis virus that strains differing by a single amino acid substitution, when inoculated together into a mouse, are competitively selected either by the liver and spleen or by neurons (9). We have recently reported that infection with multiple HCV strains results in rapid predominance of a single strain that presumably replicates in the liver and that all other strains are either eliminated or constitute a tiny fraction of circulating virions (21). It is thus possible that HCV adaptation to an extrahepatic niche may be a strategy to elude competitive exclusion by the dominant strain that replicates in the liver. (End of quote)
As can be seen this may explain problems that liver transplant patients have with clearance. It may shed light on recurrence though this is beyond my knowledge. Still it's interesting and demonstrates the utter complexity of figuring this thing out. I hope this helps some of us at least get a glimpse of what may be going on. Mike
An important question is that of how the HCV got into the CNS. In theory, HCV could gain access to the brain by way of cerebrospinal fluid as occurs in visna virus infection (12). Alternatively, and more likely, neuroinvasion is related to trafficking of infected cells of monocyte/macrophage lineage through the blood-brain barrier, in a process similar to that postulated for HIV-1 infection (28, 35). Subsequently, there could be a secondary spread of HCV to permissive resident microglial cells within the brain. Replication in the CNS could be facilitated by immunosuppression, some degree of which was likely to be present in all of our patients. This possibility is supported by the observations that while HCV negative-strand RNA is rarely detected in PBMC from normal subjects (15, 24), it is commonly found in HIV-coinfected patients or liver transplant recipients (16, 30). Moreover, HCV replication was demonstrated in hematopoietic cells inoculated into severe combined immunodeficiency mice (5). However, HCV replication in bone marrow was also found in some obviously immunocompetent subjects (29, 31).
The observed concomitant infection of the same host by two different HCV strains, each replicating in a different compartment, is probably the consequence of coinfection or superinfection with strains manifesting different tropisms for different cells. For example, it has been demonstrated for lymphocytic choriomeningitis virus that strains differing by a single amino acid substitution, when inoculated together into a mouse, are competitively selected either by the liver and spleen or by neurons (9). We have recently reported that infection with multiple HCV strains results in rapid predominance of a single strain that presumably replicates in the liver and that all other strains are either eliminated or constitute a tiny fraction of circulating virions (21). It is thus possible that HCV adaptation to an extrahepatic niche may be a strategy to elude competitive exclusion by the dominant strain that replicates in the liver. (End of quote)
As can be seen this may explain problems that liver transplant patients have with clearance. It may shed light on recurrence though this is beyond my knowledge. Still it's interesting and demonstrates the utter complexity of figuring this thing out. I hope this helps some of us at least get a glimpse of what may be going on. Mike
Thanks everyone for your words of support. It is my understanding that once something hits your brain there isn
Hi - sorry to hear about your relapse - it's pretty hard to find good news here but at least a relapse makes it more likely you'll eventually SVR than non-response (see <a href="http://hepatology2.aasldjournals.org/scripts/om.dll/serve?action=searchDB&searchDBfor=art&artType=fullfree&id=ajhep036s128">
relapse article </a> ). There's not much data data yet on retreatment of peg-intf+riba relapsers. Do you happen to remember the threshold of your viral count tests? The available choices seem to be to (a) try again now (b) wait and try again as therapy improves. With (b) one issue will be whether to follow a maintenance-level dose of ifn to slow-down liver damage. Best wishes getting through this setback.
relapse article </a> ). There's not much data data yet on retreatment of peg-intf+riba relapsers. Do you happen to remember the threshold of your viral count tests? The available choices seem to be to (a) try again now (b) wait and try again as therapy improves. With (b) one issue will be whether to follow a maintenance-level dose of ifn to slow-down liver damage. Best wishes getting through this setback.
If I'm correct about the tx not penetrating the brain barrier then yes, the virus would be there and the tx couldn't reach it. But the manner in which the tx helps us fight this infection is still unclear to me and I don't know the ramifications of the brain thing. I think this is an area of speculation insofar as recurrence is concerned. I think that if, in fact, viral copies are in the brain but not detectable through blood tests during tx, that once tx is stopped the virus would replicate and once again be detectable in the blood. There is investigation as to the effects of hep c on cognitive skills and the blood brain barrier issue has prompted speculation regarding the effects of the virus once it crosses the barrier. I've not read anything definitive in this regard - just questions and speculation. Honestly I'm not sure whether I really want to know the long term consequences of this stuff. But, being the nut I am, I'll search for it anyway. As for now I'm not going to get too worked up over it. Mike
I was watching a show (totally unrelated) about hermaphrodites the other day and one of the people that they were interviewing said that she would prefer not to be on estrogen because if she had a choice between body and brain - she would choose the brain. She thought that she didn't think clearly or deal with life well when on estrogen. I didn't understand her comment until this discussion came up today. Yeah - I am not sure if I want to know about it either - uggggg. Maybe they can alter the size of the drug in the future...who knows...right now...I have enough to think about at this early stage.
But like you - I will dig until I find something - I already have it on my list of questions for the doctor on Friday.
But like you - I will dig until I find something - I already have it on my list of questions for the doctor on Friday.
I wouldn't be too fullofhope on getting a definitive answer to that one. But, if you do, please post it. Mike
I am sorry to hear this news of yours, it is our fate
to deal with a disease whose treatment is not sure.
We just have to go through this long trip just wait
for the stastics. When I read your post, I felt bad
for you and got scared too. I wish you the best of luck.
But any way these 48 weeks were not in vain, you gave
your liver a break that it needed it.
to deal with a disease whose treatment is not sure.
We just have to go through this long trip just wait
for the stastics. When I read your post, I felt bad
for you and got scared too. I wish you the best of luck.
But any way these 48 weeks were not in vain, you gave
your liver a break that it needed it.
Hi, Mike,
This poses the question: after undetectable, should we at some point switch to - say - 5x/week regular interferon shots, since those molecules are smaller. MCN's situation is so frustrating; I sympathize deeply. I just had my 24 week Heptimax drawn, the less sensitive test was undetectable at 12 weeks. I've pretty much been visualizing myself as just cleaning up straggler viruses for the second 24 weeks (type 1b).
At the same time, it is quite possible that on Pegasys we are experiencing fewer side effects because the pegylated interferon molecules are bigger; they are not going to all the other body tissues to cause pain and inflammation there.
Tough facts to deal with with HepC:
1) We didn't get a 100% promise at the beginning of tx. When there is viral recurrance, it usually shows up quickly after the end of tx. Consider that it takes a few weeks just to get all the tx drugs out of the system, then any remaining virus has a field day. Unopposed, the VL can double roughly every 2 hours, until it reaches the level your body can hold at bay.
2) 12 week, half-way-through and end of tx "undetectables" are great, but the really important tests come after tx, at (3,) 6 and 12 months post tx. Each good test is a step in the right direction, but the fat lady doesn't sing until 12 months after tx.
MCN, best of luck in finding some safe and helpful options.
Maj Neni
This poses the question: after undetectable, should we at some point switch to - say - 5x/week regular interferon shots, since those molecules are smaller. MCN's situation is so frustrating; I sympathize deeply. I just had my 24 week Heptimax drawn, the less sensitive test was undetectable at 12 weeks. I've pretty much been visualizing myself as just cleaning up straggler viruses for the second 24 weeks (type 1b).
At the same time, it is quite possible that on Pegasys we are experiencing fewer side effects because the pegylated interferon molecules are bigger; they are not going to all the other body tissues to cause pain and inflammation there.
Tough facts to deal with with HepC:
1) We didn't get a 100% promise at the beginning of tx. When there is viral recurrance, it usually shows up quickly after the end of tx. Consider that it takes a few weeks just to get all the tx drugs out of the system, then any remaining virus has a field day. Unopposed, the VL can double roughly every 2 hours, until it reaches the level your body can hold at bay.
2) 12 week, half-way-through and end of tx "undetectables" are great, but the really important tests come after tx, at (3,) 6 and 12 months post tx. Each good test is a step in the right direction, but the fat lady doesn't sing until 12 months after tx.
MCN, best of luck in finding some safe and helpful options.
Maj Neni
Sorry to ask another question of you MS - but....
What you are saying is that the virus can get to our brains, but the cure can't - right?
Does that mean that even with TX you wouldn't test negatively if the virus got to your brain or does that mean that even after successful TX you can still have the damn virus multiplying in your brain which remains undetected during blood tests?
Also...does that also mean that the fog will get thicker and thicker...?
Sorry - need to know. If you don't want to get into here - and have already found a good "common folk" site to refer me to that would be fine.
What you are saying is that the virus can get to our brains, but the cure can't - right?
Does that mean that even with TX you wouldn't test negatively if the virus got to your brain or does that mean that even after successful TX you can still have the damn virus multiplying in your brain which remains undetected during blood tests?
Also...does that also mean that the fog will get thicker and thicker...?
Sorry - need to know. If you don't want to get into here - and have already found a good "common folk" site to refer me to that would be fine.
it looks like if she's going to sing, she'll do it by week 12 <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12821051&dopt=Abstract">
fat lady's schedule </a>. The fact that the probability of relapse drops off so fast should make the lucky ones who've gotten past the the 3-month stage sleep a little easier - but it's kind of like cancer relapse - there's always a chance.
fat lady's schedule </a>. The fact that the probability of relapse drops off so fast should make the lucky ones who've gotten past the the 3-month stage sleep a little easier - but it's kind of like cancer relapse - there's always a chance.
That is great news. For me that means I will get the word just before Christmas. Wouldn't that be a great present!!
Sorry to hear about your relapse. I have read here though about people doing more than one course of treatment. Is this not an option? Also about the brain-blood barrier. Are you all saying that the virus can replicate in the brain? I thought viral replication was in the liver only.
Since you seem to be the most informed on this blood brain barrier issue (never heard of this before, so like everyone else a little agitated) I was wondering that if you do indeed have the virus in your brain, why wouldn't it still show up in a blood test? Do you know how the case where they found the virus in the brain was discovered (not on a cadaver I hope)? Just when you think you're out of the woods.......
Thanks...Laurie
Thanks...Laurie
From the site at http://www.retroconference.org/2002/Abstract/13652.htm
"Background: Hepatitis C virus (HCV) infection is common in HIV-1-infected patients. HCV-infected patients are more likely to have changes in their physical and mental well-being than patients with liver disease of other etiology raising the possibility that the virus directly affects the central nervous system (CNS). Importantly, HCV was recently found to replicate in lymphoid cells and macrophages. To test the hypothesis that HCV can replicate in CNS, we analyzed autopsy brain tissue samples from 6 HCV-infected patients (3 were HIV+). To determine whether peripheral blood mononuclear cells (PBMC) could carry HCV across blood-brain barrier, we analyzed HCV RNA in serum, PBMC, and cerebrospinal fluid (CSF) from another group of 9 HCV-infected patients, 6 of whom were HIV+.
Methods: Negative strand HCV RNA, which is a viral replicative intermediary, was detected with a strand-specific Tth-based RT- PCR and viral sequences were compared by single-strand conformational polymorphism (SSCP), and sequencing. The analysis was conducted on the 5'untraslated region; genotype differences were confirmed by analysis of the NS5 region.
Results: HCV RNA negative strands were detected in brain tissue in 3 out of 6 patients (1 was HIV+). In 2 of these patients, serum- and brain-derived viral sequences were different and belonged to different genotypes. In 1 of these 2 patients, viral negative strands were detected in lymph node and, while being different from serum sequences, were identical to those present in the brain. Negative strand HCV RNA titers in brain tissue were one log lower than titers of the positive strand which is a ratio similar to that found in infected livers. When CSF samples were analyzed, HCV RNA was detected in 6 out of 9 cellular pellets and in 2 supernatants. HCV RNA negative strand was detected in CSF cell pellets from 2 HIV+ patients. In 2 patients who were found to harbor different viral strains in serum and PBMC, CSF-derived virus was closely related to PBMC but not to the serum strain, which suggests that HCV-infected lymphoid cells could carry the virus across the blood-brain barrier.
Conclusions: The results of the present study suggest that HCV can replicate in the central nervous system, although the consequences of this phenomenon are currently unclear. HCV-infected lymphoid cells could carry the virus across the blood-brain barrier into the CNS in a process similar to that postulated for HIV-1."
"Background: Hepatitis C virus (HCV) infection is common in HIV-1-infected patients. HCV-infected patients are more likely to have changes in their physical and mental well-being than patients with liver disease of other etiology raising the possibility that the virus directly affects the central nervous system (CNS). Importantly, HCV was recently found to replicate in lymphoid cells and macrophages. To test the hypothesis that HCV can replicate in CNS, we analyzed autopsy brain tissue samples from 6 HCV-infected patients (3 were HIV+). To determine whether peripheral blood mononuclear cells (PBMC) could carry HCV across blood-brain barrier, we analyzed HCV RNA in serum, PBMC, and cerebrospinal fluid (CSF) from another group of 9 HCV-infected patients, 6 of whom were HIV+.
Methods: Negative strand HCV RNA, which is a viral replicative intermediary, was detected with a strand-specific Tth-based RT- PCR and viral sequences were compared by single-strand conformational polymorphism (SSCP), and sequencing. The analysis was conducted on the 5'untraslated region; genotype differences were confirmed by analysis of the NS5 region.
Results: HCV RNA negative strands were detected in brain tissue in 3 out of 6 patients (1 was HIV+). In 2 of these patients, serum- and brain-derived viral sequences were different and belonged to different genotypes. In 1 of these 2 patients, viral negative strands were detected in lymph node and, while being different from serum sequences, were identical to those present in the brain. Negative strand HCV RNA titers in brain tissue were one log lower than titers of the positive strand which is a ratio similar to that found in infected livers. When CSF samples were analyzed, HCV RNA was detected in 6 out of 9 cellular pellets and in 2 supernatants. HCV RNA negative strand was detected in CSF cell pellets from 2 HIV+ patients. In 2 patients who were found to harbor different viral strains in serum and PBMC, CSF-derived virus was closely related to PBMC but not to the serum strain, which suggests that HCV-infected lymphoid cells could carry the virus across the blood-brain barrier.
Conclusions: The results of the present study suggest that HCV can replicate in the central nervous system, although the consequences of this phenomenon are currently unclear. HCV-infected lymphoid cells could carry the virus across the blood-brain barrier into the CNS in a process similar to that postulated for HIV-1."
best wishes for a week-12-clear lab report under your tree! That's an interesting abstract you posted. Replication outside the liver is known but the fact that the +/- RNA ratios in brain tissue is the same as for liver cells would suggests the virus is replicating as fast there as in the liver. Not good news - though it may finally provide support for some of "self-reported" neuro/psychiatric disorders associated with hcv.
MCN,
I am sorry to hear about your relapse. Hopefully you have bought yourself more time to wait for a better tx to come along. After reading what the others have posted I am curious if you feel that you have had any central nervous system issues?
To the other posters, something to think over,
If HCV were replicating in the CNS would it be necessary for the tx to also get there to battle the virus? From what I understand it is not the tx that kills the virus but it is the tx that boost our immune systems which in turn kill the virus. The components of our immune system cross the blood brain barrier, don't they? Does anyone know?
I am sorry to hear about your relapse. Hopefully you have bought yourself more time to wait for a better tx to come along. After reading what the others have posted I am curious if you feel that you have had any central nervous system issues?
To the other posters, something to think over,
If HCV were replicating in the CNS would it be necessary for the tx to also get there to battle the virus? From what I understand it is not the tx that kills the virus but it is the tx that boost our immune systems which in turn kill the virus. The components of our immune system cross the blood brain barrier, don't they? Does anyone know?
Just wanted to say I'm sorry to hear this news. As everyone, hoping and praying there is new tx down the road.
Great...
(said very sarcastically) ;)
Thanks for the information - I will add that to my list of things to research.
You are a great source of info for me - I appreciate you being here and sharing your knowledge.
(said very sarcastically) ;)
Thanks for the information - I will add that to my list of things to research.
You are a great source of info for me - I appreciate you being here and sharing your knowledge.
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