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HCV infection in heavy alcohol users. Interesting Study.
I have long speculated that heavy alcohol use might just cause some sort of 'activation' of the HCV virus in certain persons that might have a suppressed, or latent form of the virus somewhere in their systems. Possibly this heavy alcohol use could cause the emergence of a full blown, chronic HCV infection, newly detectable by standard blood testing. I just came across this NIH study, and article from a few years ago, which appeared in Hepatology. Notice, way down in the article, the comments about researchers confusion over alcohol's role in the acquisition of HCV. They refer to those without other risk factors, and still seem to have not been able to clarify why there is such a disproportionate number of alcoholics who become HCV positive. Remember, these are alcoholich who have no IVDU or transfusion history. My idea is that some people probably do carry a subdetectable HCV virus, that is kept under immune system control, and is not provoking a humoral antibody response. These might be the people who 'come down with HCV' after chronic heavy drinking. Just my explanation of this riddle. Here is the article:
Alcohol Increases Hepatitis C Virus in Human Cells
Drinking May Compromise Treatment Success
A team of NIH-supported researchers today report that alcohol increases replication of the hepatitis C virus (HCV) in human cells and, by so doing, may contribute to the rapid course of HCV infection. The researchers tested the actions of alcohol in HCV replicon — viral HCV-ribonucleic acid or HCV-RNAs that, when introduced into human liver cell lines, replicate to high levels. In separate laboratory experiments they showed that
alcohol increases HCV replication at least in part by upregulating a key cellular regulator of immune pathways and function known as nuclear factor kappa B (NF-κB);
alcohol inhibits the anti-HCV effect of interferon-alpha (INF-α) therapy; and
treatment with the opioid antagonist naltrexone abolishes alcohol actions.
Wenzhe Ho, M.D., and Steven D. Douglas, M.D., Department of Pediatrics, University of Pennsylvania, and the Joseph Stokes, Jr. Research Institute at The Children's Hospital of Philadelphia, and colleagues in the Department of Psychiatry, University of Pennsylvania School of Medicine report their results in the July 2003 issue of Hepatology (Volume 38, Number 1, pages 57-65).
Speculating that alcohol somehow promotes HCV expression, the researchers relied on a recently available cellular system for studying the dynamics of virus replication (developed and provided to the investigators by Drs. C. M. Rice, The Rockefeller University, and Christoph Seeger, Fox Chase Cancer Center) to demonstrate for the first time that alcohol enhances HCV replicon expression at both the messenger RNA and protein levels. In the cell lines used for the study, the research team also showed that alcohol activation of NF-κB was responsible for increasing HCV expression. "Although the replicon system mimics only some aspects of HCV replication, we have identified at least a likely mechanism whereby alcohol increases viral load and thus may become an important cofactor in HCV severity," Dr. Douglas said.
"These findings are immediately useful to clinicians for counseling HCV-positive patients about alcohol use," said Ting-Kai Li, M.D., Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA). "For clinical and basic scientists, they raise new research questions, many of which no doubt will be explored using the model and methods introduced today." NIAAA supported the experiments through a grant to Dr. Douglas, whose work also was supported by the National Institute of Mental Health and the National Institute on Drug Abuse (NIDA). The NIAAA and NIDA supported Dr. Ho's work on the study.
HCV is an RNA virus of the flavivirus family that infects about 4 million U.S. residents and produces some 30,000 new infections each year. HCV typically escapes clearance by the immune system and leads to persistent, chronic infection in 70 to 85 percent of infected individuals, of whom fewer than 50 percent respond to IFN-α, the HCV therapy of choice. Over the long term, HCV infection can lead to cirrhosis, liver failure, and liver cancer. As a group, HCV-infected individuals are the major recipients of liver transplantation.
Clinicians have long observed a high incidence of HCV infection in heavy drinkers, including those without other risk factors such as intravenous drug abuse or history of blood transfusions. In addition, the virus is more likely to persist in heavy drinkers and to lead to such complications as cirrhosis and liver cancer. Suspected mechanisms for the latter effects include alcohol's capacity to compromise immune function and enhance oxidative stress. The role of alcohol use in HCV acquisition has been more of a mystery.
During the 1990s, several studies reported higher blood levels of HCV in drinkers than abstainers and in habitual than infrequent drinkers. Further, drinking reduction was shown to diminish the number of virus particles in the blood. These observations led Dr. Douglas and his colleagues to pursue the role of alcohol in HCV replication.
Using the same replicon, Drs. Ho, Douglas and their colleagues also demonstrated that alcohol compromises IFN-α action against HCV and explored a plausible mechanism for alcohol's role in HCV expression. Alcohol interferes with endogenous opiates, which have a key role in its addictive properties. The researchers found that the opiate receptor antagonist naltrexone, better known for its utility in helping alcoholism treatment patients to avoid relapse, not only blocked the promoting effect of alcohol on HCV expression but also diminished alcohol activation of NF-κB in these cells. "These data strongly suggest that activation of the endogenous opioid system is implicated in alcohol-induced HCV expression," the authors conclude.
For an interview with Dr. Douglas, please telephone (215) 590-1978; for an interview with Dr. Ho, please telephone (215) 590-4462. For an interview with NIAAA staff members, please contact the NIAAA Press Office. Publications and additional alcohol research information are available at www.niaaa.nih.gov.
The National Institute on Alcohol Abuse and Alcoholism, a component of the National Institutes of Health, U.S. Department of Health and Human Services, conducts and supports approximately 90 percent of U.S. research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems and disseminates research findings to science, practitioner, policy making, and general audiences.
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Alcohol Increases Hepatitis C Virus in Human Cells
Drinking May Compromise Treatment Success
A team of NIH-supported researchers today report that alcohol increases replication of the hepatitis C virus (HCV) in human cells and, by so doing, may contribute to the rapid course of HCV infection. The researchers tested the actions of alcohol in HCV replicon — viral HCV-ribonucleic acid or HCV-RNAs that, when introduced into human liver cell lines, replicate to high levels. In separate laboratory experiments they showed that
alcohol increases HCV replication at least in part by upregulating a key cellular regulator of immune pathways and function known as nuclear factor kappa B (NF-κB);
alcohol inhibits the anti-HCV effect of interferon-alpha (INF-α) therapy; and
treatment with the opioid antagonist naltrexone abolishes alcohol actions.
Wenzhe Ho, M.D., and Steven D. Douglas, M.D., Department of Pediatrics, University of Pennsylvania, and the Joseph Stokes, Jr. Research Institute at The Children's Hospital of Philadelphia, and colleagues in the Department of Psychiatry, University of Pennsylvania School of Medicine report their results in the July 2003 issue of Hepatology (Volume 38, Number 1, pages 57-65).
Speculating that alcohol somehow promotes HCV expression, the researchers relied on a recently available cellular system for studying the dynamics of virus replication (developed and provided to the investigators by Drs. C. M. Rice, The Rockefeller University, and Christoph Seeger, Fox Chase Cancer Center) to demonstrate for the first time that alcohol enhances HCV replicon expression at both the messenger RNA and protein levels. In the cell lines used for the study, the research team also showed that alcohol activation of NF-κB was responsible for increasing HCV expression. "Although the replicon system mimics only some aspects of HCV replication, we have identified at least a likely mechanism whereby alcohol increases viral load and thus may become an important cofactor in HCV severity," Dr. Douglas said.
"These findings are immediately useful to clinicians for counseling HCV-positive patients about alcohol use," said Ting-Kai Li, M.D., Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA). "For clinical and basic scientists, they raise new research questions, many of which no doubt will be explored using the model and methods introduced today." NIAAA supported the experiments through a grant to Dr. Douglas, whose work also was supported by the National Institute of Mental Health and the National Institute on Drug Abuse (NIDA). The NIAAA and NIDA supported Dr. Ho's work on the study.
HCV is an RNA virus of the flavivirus family that infects about 4 million U.S. residents and produces some 30,000 new infections each year. HCV typically escapes clearance by the immune system and leads to persistent, chronic infection in 70 to 85 percent of infected individuals, of whom fewer than 50 percent respond to IFN-α, the HCV therapy of choice. Over the long term, HCV infection can lead to cirrhosis, liver failure, and liver cancer. As a group, HCV-infected individuals are the major recipients of liver transplantation.
Clinicians have long observed a high incidence of HCV infection in heavy drinkers, including those without other risk factors such as intravenous drug abuse or history of blood transfusions. In addition, the virus is more likely to persist in heavy drinkers and to lead to such complications as cirrhosis and liver cancer. Suspected mechanisms for the latter effects include alcohol's capacity to compromise immune function and enhance oxidative stress. The role of alcohol use in HCV acquisition has been more of a mystery.
During the 1990s, several studies reported higher blood levels of HCV in drinkers than abstainers and in habitual than infrequent drinkers. Further, drinking reduction was shown to diminish the number of virus particles in the blood. These observations led Dr. Douglas and his colleagues to pursue the role of alcohol in HCV replication.
Using the same replicon, Drs. Ho, Douglas and their colleagues also demonstrated that alcohol compromises IFN-α action against HCV and explored a plausible mechanism for alcohol's role in HCV expression. Alcohol interferes with endogenous opiates, which have a key role in its addictive properties. The researchers found that the opiate receptor antagonist naltrexone, better known for its utility in helping alcoholism treatment patients to avoid relapse, not only blocked the promoting effect of alcohol on HCV expression but also diminished alcohol activation of NF-κB in these cells. "These data strongly suggest that activation of the endogenous opioid system is implicated in alcohol-induced HCV expression," the authors conclude.
For an interview with Dr. Douglas, please telephone (215) 590-1978; for an interview with Dr. Ho, please telephone (215) 590-4462. For an interview with NIAAA staff members, please contact the NIAAA Press Office. Publications and additional alcohol research information are available at www.niaaa.nih.gov.
The National Institute on Alcohol Abuse and Alcoholism, a component of the National Institutes of Health, U.S. Department of Health and Human Services, conducts and supports approximately 90 percent of U.S. research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems and disseminates research findings to science, practitioner, policy making, and general audiences.
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I am really doubtful that those who drank through tx and SVR'ed fit the chronic, extreme alcoholic/abuse pattern. I think that they are referring to very heavy bouts of drinking, for prolonged periods of time. Someone doing that on tx would not be on tx for long, and I also do not think that sort of drinking behavior would result in SVR. I think many have also used alcohol after SVR, and do not seem to be compromising their SVR, BUT...I would be concerned for those that went back to a 'heavy and chronic abuse' pattern, and whether it could potentiaqlly impact their SVR, as in one of the stories from another forum, related above.
If indeed the persistent HCV after SVR research is valid....and if there really is more of a 'remission' rather than total and complete eradication after SVR, then I would have to believe that there would be mechanisms or behaviors that could cause a re-emergence of the virus. This is a very little understood area, and there is almost no real research on whether or not some of the 'relapses' that have occurred in long term SVR's were really true 'relapses' or re-infections. Many like to ASSUME that they must have been re-infections, but that is extremely unscientific, and there is no supporting evidence for either conclusion. Much more study is needed, and also on the persistent HCV research that has been published. We really do not know anything about what the ramifications might be, or even whether the research is proven valid for all or most SVR's.
The 'Occult" HCV issue is even less studied, and less understood. There are some that have HCV in the liver, but not in the blood. Some have negative PCR's and others have negative HCV antibody tests. It is a very gray area, and I do not think anyone knows why the virus infects in this manner, or HOW it can do it without a blood viral load.
This is exactly why I do not buy all the 'cut and dried' answers that many have regarding HCV. It is really a work in progress, and new findings hit the press every year. I would never pretend to know too much about HCV. Even if some doctors are prone to doing that themselves.
DoubleDose
If indeed the persistent HCV after SVR research is valid....and if there really is more of a 'remission' rather than total and complete eradication after SVR, then I would have to believe that there would be mechanisms or behaviors that could cause a re-emergence of the virus. This is a very little understood area, and there is almost no real research on whether or not some of the 'relapses' that have occurred in long term SVR's were really true 'relapses' or re-infections. Many like to ASSUME that they must have been re-infections, but that is extremely unscientific, and there is no supporting evidence for either conclusion. Much more study is needed, and also on the persistent HCV research that has been published. We really do not know anything about what the ramifications might be, or even whether the research is proven valid for all or most SVR's.
The 'Occult" HCV issue is even less studied, and less understood. There are some that have HCV in the liver, but not in the blood. Some have negative PCR's and others have negative HCV antibody tests. It is a very gray area, and I do not think anyone knows why the virus infects in this manner, or HOW it can do it without a blood viral load.
This is exactly why I do not buy all the 'cut and dried' answers that many have regarding HCV. It is really a work in progress, and new findings hit the press every year. I would never pretend to know too much about HCV. Even if some doctors are prone to doing that themselves.
DoubleDose
I wonder about those that I have heard that drank through tx and afterwards and SVR'ed. How does this fit the pattern? Occult or not, they seemed to not fit this mold.
Thanks for your post. It refreshed my memory of why I generally stay clear of these threads. Actually, this is probably the first one in a long time that had a few “thought through” responses and was not over run with emotion.
I'm not sure of this, but I think there are two different issues being discussed on this thread...one is if alcohol causes HCV to worsen (that of course has so many variables, who is drinking, how much, etc etc...there are plenty of studies out there that point to this)..and another is if you are SVR already, will huge amounts of alcohol cause a minute amount of dormant virus to rear it's ugly head again, which is only theoretical...
I’ve recently had this conversation with my Gastro. Who works very close with one of the leading Hepatitis Spec. In this area. He said there is no proof (only Theories) that alcohol causes HCV to replicate. Of course he made it clear, no one with HCV, Severe Liver Damage, or During Treatment, should even entertain the thought of consuming alcohol.
I look at some these HCV studies in the same manner as I look at how some preachers use the Bible. They twist it and add enough opinion, to can make it say anything they want to.
I look at some these HCV studies in the same manner as I look at how some preachers use the Bible. They twist it and add enough opinion, to can make it say anything they want to.
I was referring to getting hammered after SVR, not casual drinking, and I mean a few here and there...sometimes my definition of casual is not someone else's definition...lol...
this woman I was talking about was finishing off bottles of booze...that ought to get a few systems going wonky...I really don't know the answers to these questions, and I'm not qualified to make conclusions by any means...
I do find DD's theories compelling though....and let's face it, when I used to be more interested in these things, I used to ask people all the time...whether they SVRed or relapsed, whatever...from a trial or private treatment, did your doc follow up with you? Did the drug company follow up with you? Most people I ever asked said that no, the trial docs never followed up with them or their docs..
.if they wanted to re-treat or whatever...the patients are the ones who resumed contact...so that kind of makes me think that all these professionals involved do little follow up with patients, so maybe there isn't a whole lot follow up data. Which begs the question, what does go on with many people once they go off treatment? They should do more studies.
this woman I was talking about was finishing off bottles of booze...that ought to get a few systems going wonky...I really don't know the answers to these questions, and I'm not qualified to make conclusions by any means...
I do find DD's theories compelling though....and let's face it, when I used to be more interested in these things, I used to ask people all the time...whether they SVRed or relapsed, whatever...from a trial or private treatment, did your doc follow up with you? Did the drug company follow up with you? Most people I ever asked said that no, the trial docs never followed up with them or their docs..
.if they wanted to re-treat or whatever...the patients are the ones who resumed contact...so that kind of makes me think that all these professionals involved do little follow up with patients, so maybe there isn't a whole lot follow up data. Which begs the question, what does go on with many people once they go off treatment? They should do more studies.
Enter a major trigger (heavy alcohol use, morphine/ opiate use, etc, as the article relates), and BAM, just like Chef Emeril you have the full blown Souffle!
I believe that you are right and it's a personally sensible thing. If you think about it your immune system I guess would be so busy working out all that **** out of your body that it might lessen its grip while the alcohol or drugs was helping it to replicate.
They were talking about bed bugs this morning on the news and said they can CARRY HepB / HIV but not transmit it. I thought hey why not? They said that the hep would stay alive for at least one hour after they bit the host. So I guess it's back to the question "if a mosquito can transmit malaria why not HIV or HEP" - just meaning it gave me pause to wonder how many ways can you actually GET HepC that they don't really know about yet.
I mean are the SURE?
All in all a very great article and discussion.
I believe that you are right and it's a personally sensible thing. If you think about it your immune system I guess would be so busy working out all that **** out of your body that it might lessen its grip while the alcohol or drugs was helping it to replicate.
They were talking about bed bugs this morning on the news and said they can CARRY HepB / HIV but not transmit it. I thought hey why not? They said that the hep would stay alive for at least one hour after they bit the host. So I guess it's back to the question "if a mosquito can transmit malaria why not HIV or HEP" - just meaning it gave me pause to wonder how many ways can you actually GET HepC that they don't really know about yet.
I mean are the SURE?
All in all a very great article and discussion.
hmmm...all of this seems like a pretty convincing argument to stay off the booze if I ever svr.
I am basically stating the second explanation that you described. That there are people with the virus already in their systems, but undetected, and in a more or less dormant state. The alcohol would trigger the virus into a full blown infection.
I also leave room for how they got the virus 'into' their systems initially, since I think there is not enough understanding on the realm of possibilities for this, at this point. Could a person receive the virus through a compartmentalized transmission (fluids, birth transmission, sexual, etc.) in which the virus does not trigger any humoral antibody alarms, but remains silently replicating in a contained reservoir? There is already huge research evidence that the virus exists and replicates in lymphatic glands and cells, potentially also in salivary glands, etc. So possibly there could be a 'cellular' level transmission that remains contained by the cellular immune system, and only becomes a full blown systemwide infection after some major triggering event....like the alcohol abuse behaviors described in the research article...which then allow the previously contained, compartmentalized virus to replicate. Maybe there are mechanisms for controlling minute amounts of virus in the body, as in SVR's and spontaneous clearers, where the person no longer appears to be infected, and has no PCR load, BUT the virus indeed is able to be found in very small amounts, in some compartments in the body, over many years.
My conjecture is that there may be others out there exposed in some way to the virus, that have never suffered the "Acute" infection, and whose system has already quickly contained and suppressed any exposure to the virus, and now holds it in-check in an ongoing basis. Enter a major trigger (heavy alcohol use, morphine/ opiate use, etc, as the article relates), and BAM, just like Chef Emeril you have the full blown Souffle!
So, maybe there are people scattered throughout the population in small or large percentages, who have already been exposed to the virus, may have small amounts in their systems with no viral load, and no detectable antibodies in the blood, who will never suffer an HCV infection as we know it, UNLESS they experience some triggering event. Maybe this is why so many people who have absolutely no IVDU, transfusions, surgeries, tattoos, etc. get diagnosed with HCV and literally have no idea how they could have gotten it. And maybe this also is why so many more alcohol abusers seem to get infected than the rest of the 'non-alcohol-abusing population.
I hope this clearly explains my comments, and some of the conjecture that I have added regarding the research article.
DoubleDose
I also leave room for how they got the virus 'into' their systems initially, since I think there is not enough understanding on the realm of possibilities for this, at this point. Could a person receive the virus through a compartmentalized transmission (fluids, birth transmission, sexual, etc.) in which the virus does not trigger any humoral antibody alarms, but remains silently replicating in a contained reservoir? There is already huge research evidence that the virus exists and replicates in lymphatic glands and cells, potentially also in salivary glands, etc. So possibly there could be a 'cellular' level transmission that remains contained by the cellular immune system, and only becomes a full blown systemwide infection after some major triggering event....like the alcohol abuse behaviors described in the research article...which then allow the previously contained, compartmentalized virus to replicate. Maybe there are mechanisms for controlling minute amounts of virus in the body, as in SVR's and spontaneous clearers, where the person no longer appears to be infected, and has no PCR load, BUT the virus indeed is able to be found in very small amounts, in some compartments in the body, over many years.
My conjecture is that there may be others out there exposed in some way to the virus, that have never suffered the "Acute" infection, and whose system has already quickly contained and suppressed any exposure to the virus, and now holds it in-check in an ongoing basis. Enter a major trigger (heavy alcohol use, morphine/ opiate use, etc, as the article relates), and BAM, just like Chef Emeril you have the full blown Souffle!
So, maybe there are people scattered throughout the population in small or large percentages, who have already been exposed to the virus, may have small amounts in their systems with no viral load, and no detectable antibodies in the blood, who will never suffer an HCV infection as we know it, UNLESS they experience some triggering event. Maybe this is why so many people who have absolutely no IVDU, transfusions, surgeries, tattoos, etc. get diagnosed with HCV and literally have no idea how they could have gotten it. And maybe this also is why so many more alcohol abusers seem to get infected than the rest of the 'non-alcohol-abusing population.
I hope this clearly explains my comments, and some of the conjecture that I have added regarding the research article.
DoubleDose
A team of NIH-supported researchers today report that alcohol increases replication of the hepatitis C virus (HCV) in human cells and, by so doing, may contribute to the rapid course of HCV infection.
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I've always believed that this is how many of us who were more than "casual" drinkers could reach a high stage in the same amount of time as another who does not drink. Increasing the replication raises the liver enzymes and voila....major cell death and increasing stages. Duh, easy point.
Of course - there can be people who treat and completely annhiliate the virus and are truly UND, then there can be others who "appear" to be completely UND - are not - go back to drinking and the virus springs back into heavy replication.
Once again it would seem to be to be completely subjective to what is going on in the persons particular body - true UND or not. SVR would therefore mean to me "under control barring no unforeseen complications" - meaning you could have virus - albeit undetectible levels of it but still have systemic virological response - but NOT truly be UND.
Then the virus would have the perfect opportunity if one were to imbibe and not truly be UND (compared to SVR) and begin its replicating wonderland of freefall.
I hope that made some sort of sense. SVR with TRUE UND level of ZERO or SVR with UND levels. And I guess since there is no test that sensitive one could never know until it's too late.
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I've always believed that this is how many of us who were more than "casual" drinkers could reach a high stage in the same amount of time as another who does not drink. Increasing the replication raises the liver enzymes and voila....major cell death and increasing stages. Duh, easy point.
Of course - there can be people who treat and completely annhiliate the virus and are truly UND, then there can be others who "appear" to be completely UND - are not - go back to drinking and the virus springs back into heavy replication.
Once again it would seem to be to be completely subjective to what is going on in the persons particular body - true UND or not. SVR would therefore mean to me "under control barring no unforeseen complications" - meaning you could have virus - albeit undetectible levels of it but still have systemic virological response - but NOT truly be UND.
Then the virus would have the perfect opportunity if one were to imbibe and not truly be UND (compared to SVR) and begin its replicating wonderland of freefall.
I hope that made some sort of sense. SVR with TRUE UND level of ZERO or SVR with UND levels. And I guess since there is no test that sensitive one could never know until it's too late.
I am very confused. Are you saying that drinking might CAUSE the hcv virus to spontaneously appear? I hope not because spontaneous generation was debunked by Louis Pasteur in the 19th century, and his findings are the cornerstone of microbiology and germ theory (remember biology class).
Or are you saying that people can walk around with a tiny amount of virus in their system which alcohol helps replicate and then become chronic? This seems probable considering all of the people that 'clear' the virus on their own. I think that people experiencing alcohol seemingly causing the hcv infection could be from this group of people that cleared the virus initially. That makes sense to me, but then they still had to get the initial infection from a blood to blood contact right?
This harks back to the good old debate as to whether are bodies ever really get rid of the virus completely.
Anyway, please clarify, because it seems like you are proposing both scenarios...
Or are you saying that people can walk around with a tiny amount of virus in their system which alcohol helps replicate and then become chronic? This seems probable considering all of the people that 'clear' the virus on their own. I think that people experiencing alcohol seemingly causing the hcv infection could be from this group of people that cleared the virus initially. That makes sense to me, but then they still had to get the initial infection from a blood to blood contact right?
This harks back to the good old debate as to whether are bodies ever really get rid of the virus completely.
Anyway, please clarify, because it seems like you are proposing both scenarios...
I just said that Schiff's explanation -- per my quote -- seemed more plausible -- so you must admit I have good company :) That doesn't mean I'm selectively throwing out anything or even discounting what you are theorizing. I DO keep an "open and keenly inquisitive mind" or so I tell women at bars (sipping diet coke, of course) trying to
impress:) Hope this finds you well, and please keep the thoughts coming but please also accept respectful alternative/counter theories, as hopefully mine are presented.
-- Jim
impress:) Hope this finds you well, and please keep the thoughts coming but please also accept respectful alternative/counter theories, as hopefully mine are presented.
-- Jim
I have also read, (and re-read) a number of accounts of people who were never associated with IVDU, or known blood exchange risk factors, who were certain that their HCV was diagnosed after a long period of heavy drinking. The woman you are referring to sounds like a similar story, but one that could also be followed and verified by her doctors.
And the last thing that I want to do is create controversy by speculating....BUT...reading the research article again, and thinking back to a host of other articles and researcher studies that have made similar comments about HCV acquisition seeming to somehow 'relate to ' heavy, prolonged alcohol abuse', I have to follow THEIR comments (Jim, please note) and come up with at least one plausible explanation for this phenomenon, other than thinking that all these subjects are just 'out and out' lying about previous risk factors.
I really don't think that it is very much of a stretch to picture people who are similar to the spontaneous clearers of HCV...that is, they have a very low level, persistent virus in their systems (as do the spontaneous clearers, and we SVR's by the way, as many researchers have demonstrated), which is and has been kept in check all their lives. They might begin drinking in high school, college, or in their early working years, and some become binge drinkers, or chronic abusers. The virus might not have shown up on liver tests, NOR even be detectable on anti-HCV antibody testing, because they may react in the same way as many with Occult HCV...that is, with no detectable antibodies to HCV. They might also be negative on blood PCR testing as many occult HCV carriers. No doctor or researcher has yet figured out how this works, but it does happen regularly.
So, these people who have been somewhow exposed to HCV at low levels, and never developed an active, or acute, or chronic HCV detectable infection, may well convert somehow into now having active and chronic HCV infections, sometime after this heavy drinking pattern is established. This is what the research article seems to be alluding to in various ways...both in their description of the scientific mechanism for alcohol causing a 'triggering of HCV replication and infection', AND in their inductive reasoning regarding the numbers of HCV infected alcohol abusers WITHOUT any prior risk factors.
Now, of course, some people may 'selectively' choose to throw out the statistics showing the lack of risk factors (Jim), but then you cannot accept other research statistics on any HCV behaviors, since anyone might also lie about any other issue, as well. You can't accept the statistical findings that you agree with and explain, and then toss out the research study findings, or statistical analyses that you don't like or agree with, or easily explain. This leads to selective analysis, and undercuts the validity and use of ANY research statistics.
Of course, I still believe that the current research and knowledge-base regarding HCV is nowhere near complete, and that there are many things that we will eventually learn about HCV that we might currently find surprising or even shocking. This alcohol research opens some new doors, but still fails to move to the next step and try to find out how and why this is happening. The researchers currently studying 'persistent virus after SVR and spontaneous clearance' are also moving rapidly along these new frontiers...as are the researchers who are now determining that many diseases are actually often CAUSED by HCV, like Diabetes, EMC, reactive arthritis, many skin conditions, some depression, behavioral abnormalities, variations of Sjogren's Syndrome, cases of Cerebral Hemmorhage, etc.
Just ten years ago both lay persons and doctors would have scoffed at these HCV connections. Why just fifteen years ago, most doctors felt that HCV was entirely asymptomatic, and ONLY caused liver damage!!! Most people might well live forever (full, event-free lives) with HCV...so they thought (recently also debunked)
My only point on all of this is that we MUST keep and open and keenly inquisitive mind, when it comes to HCV questions and studies. We cannot be afraid of the truth! Just because the doctors have a set of 'assumptions' about the virus today, has NO bearing on what their assumptions might include ten to twenty years from now. There is just a lot more to understand. This is a work in progress, to be sure.
Have a great week all of you!!!! Stay well, and happy!
DoubleDose
And the last thing that I want to do is create controversy by speculating....BUT...reading the research article again, and thinking back to a host of other articles and researcher studies that have made similar comments about HCV acquisition seeming to somehow 'relate to ' heavy, prolonged alcohol abuse', I have to follow THEIR comments (Jim, please note) and come up with at least one plausible explanation for this phenomenon, other than thinking that all these subjects are just 'out and out' lying about previous risk factors.
I really don't think that it is very much of a stretch to picture people who are similar to the spontaneous clearers of HCV...that is, they have a very low level, persistent virus in their systems (as do the spontaneous clearers, and we SVR's by the way, as many researchers have demonstrated), which is and has been kept in check all their lives. They might begin drinking in high school, college, or in their early working years, and some become binge drinkers, or chronic abusers. The virus might not have shown up on liver tests, NOR even be detectable on anti-HCV antibody testing, because they may react in the same way as many with Occult HCV...that is, with no detectable antibodies to HCV. They might also be negative on blood PCR testing as many occult HCV carriers. No doctor or researcher has yet figured out how this works, but it does happen regularly.
So, these people who have been somewhow exposed to HCV at low levels, and never developed an active, or acute, or chronic HCV detectable infection, may well convert somehow into now having active and chronic HCV infections, sometime after this heavy drinking pattern is established. This is what the research article seems to be alluding to in various ways...both in their description of the scientific mechanism for alcohol causing a 'triggering of HCV replication and infection', AND in their inductive reasoning regarding the numbers of HCV infected alcohol abusers WITHOUT any prior risk factors.
Now, of course, some people may 'selectively' choose to throw out the statistics showing the lack of risk factors (Jim), but then you cannot accept other research statistics on any HCV behaviors, since anyone might also lie about any other issue, as well. You can't accept the statistical findings that you agree with and explain, and then toss out the research study findings, or statistical analyses that you don't like or agree with, or easily explain. This leads to selective analysis, and undercuts the validity and use of ANY research statistics.
Of course, I still believe that the current research and knowledge-base regarding HCV is nowhere near complete, and that there are many things that we will eventually learn about HCV that we might currently find surprising or even shocking. This alcohol research opens some new doors, but still fails to move to the next step and try to find out how and why this is happening. The researchers currently studying 'persistent virus after SVR and spontaneous clearance' are also moving rapidly along these new frontiers...as are the researchers who are now determining that many diseases are actually often CAUSED by HCV, like Diabetes, EMC, reactive arthritis, many skin conditions, some depression, behavioral abnormalities, variations of Sjogren's Syndrome, cases of Cerebral Hemmorhage, etc.
Just ten years ago both lay persons and doctors would have scoffed at these HCV connections. Why just fifteen years ago, most doctors felt that HCV was entirely asymptomatic, and ONLY caused liver damage!!! Most people might well live forever (full, event-free lives) with HCV...so they thought (recently also debunked)
My only point on all of this is that we MUST keep and open and keenly inquisitive mind, when it comes to HCV questions and studies. We cannot be afraid of the truth! Just because the doctors have a set of 'assumptions' about the virus today, has NO bearing on what their assumptions might include ten to twenty years from now. There is just a lot more to understand. This is a work in progress, to be sure.
Have a great week all of you!!!! Stay well, and happy!
DoubleDose
I acquired Hep C from a blood to blood wound (home invasion, essentially a fight), and I have theorized before on here, that this may be a large reason why this virus has lasted so long throughout history, given that blood is the only means of transmission. The "war factor" if you will. The blackouts may very well have been the cause.
Before I was sober I was drinking heavy, and several times I woke up covered in blood, and had no memory what has happen for days (blackouted), most of the times i had felt from a bicykle or something, ( finded out after investingation) rarely but sometimes I had been in a fight.And the people i was associatid with , were of the same calibre.They were also bleeding from time to time, so the infection risk must be higher blood to blood by wounds, in that categori then among other groups of peoble.
As who I got infected it was from the needle, injected speed.
As who I got infected it was from the needle, injected speed.
This was just released Jan23
http://www.ncbi.nlm.nih.gov/pubmed/18216180?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
A major cause of liver cirrhosis and hepatocarcinoma is chronic infection by hepatitis C virus. Ethanol consumption is the most significant environmental factor that exacerbates the progression of chronic hepatitis C to liver cirrhosis and hepatocarcinoma, perhaps due to increased cytokine secretion together with increased lipid peroxidation.
http://www.ncbi.nlm.nih.gov/pubmed/18216180?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
A major cause of liver cirrhosis and hepatocarcinoma is chronic infection by hepatitis C virus. Ethanol consumption is the most significant environmental factor that exacerbates the progression of chronic hepatitis C to liver cirrhosis and hepatocarcinoma, perhaps due to increased cytokine secretion together with increased lipid peroxidation.
Dr. Schiff's speculation in this 1994 presentation seems more plausible than alcohol somehow activating a sleeping virus. It also might be added that lower socioeconomic status may also present other risks as well -- such as unlicensed tatoo parlours, and even sub-par medical clinics. Also, I'm assuming that the way they ruled out IV drug use was from questionaires which brings up the point how honest people were in their answers.
"...Socioeconomic status is a known risk factor for HCV and is probably a factor among alcoholic patients. African Americans and Hispanics have a higher prevalence of alcohol abuse and HCV.[26] In addition, African Americans have a higher prevalence of genotype 1b HCV and poor response to interferon treatment..."
http://www.medscape.com/viewarticle/488940_2
"...Socioeconomic status is a known risk factor for HCV and is probably a factor among alcoholic patients. African Americans and Hispanics have a higher prevalence of alcohol abuse and HCV.[26] In addition, African Americans have a higher prevalence of genotype 1b HCV and poor response to interferon treatment..."
http://www.medscape.com/viewarticle/488940_2
as far as progressing and damage, etc etc...I do think that taking good care of yourself bodes really well for a person, I have known I had this since 01...and Im still in good shape relative to liver damage, and I have good labs (my viral load has never been over 200,000 which might not mean a whole lot I realize) and my alts are in the low 30s 20s...I happen to think that if I would of kept up what I was doing in my twenties? There would be no way I'd be 54 now and in the shape I am in now. No way. That's just my personal feeling.
Of course there will always be anomalies...the lady who lived in my building who was 80 and she smoked till she was 78, and was a binge drinker (got flat on her a$$ drunk for 5 days at a time, then she wouldn't drink for 4 to 6 months, alcoholism can express itself this way too, if she had been a daily drunk, she prob wouldn't have fared as well)...
there will always be people with these kind of constitutions...but I think, for the most part, you're liver is a filtering organ, the more cr@p you make it filter, the more stressed it is, add to that an ongoing virus attacking it...most people will progress a lot faster if they keep up a bad lifestyle, but not all it seems.
And then there the poor people who take excellent care of themselves, and they progress rapidly anyway, but they seem to be in the very minority. These are conclusions I've made by just reading a long time too. Just my take.
Of course there will always be anomalies...the lady who lived in my building who was 80 and she smoked till she was 78, and was a binge drinker (got flat on her a$$ drunk for 5 days at a time, then she wouldn't drink for 4 to 6 months, alcoholism can express itself this way too, if she had been a daily drunk, she prob wouldn't have fared as well)...
there will always be people with these kind of constitutions...but I think, for the most part, you're liver is a filtering organ, the more cr@p you make it filter, the more stressed it is, add to that an ongoing virus attacking it...most people will progress a lot faster if they keep up a bad lifestyle, but not all it seems.
And then there the poor people who take excellent care of themselves, and they progress rapidly anyway, but they seem to be in the very minority. These are conclusions I've made by just reading a long time too. Just my take.
I agree with your post. I just find it curious. If this woman was being truthful, and she really emphasized that she had gone through a year of treatment and she completely knew what the blood to blood risks were, she did no drugs (she said) while she was getting hammered...maybe the loads of alcohol reactivated an occult virus?, that would never have come up otherwise?
I have no idea, there is no way of proving anything, I just find it interesting. She claimed that there have been other reported cases like this, but I don't have the wherewithal to look all that up. Or she could be totally full of it, she just didn't strike me like that though, she was very kind and answered questions in a legit way for people on the board, etc etc...
I have no idea, there is no way of proving anything, I just find it interesting. She claimed that there have been other reported cases like this, but I don't have the wherewithal to look all that up. Or she could be totally full of it, she just didn't strike me like that though, she was very kind and answered questions in a legit way for people on the board, etc etc...
I haven't drank since 1994 (when I was diagnosed), except on ONE occasion when I did try to have 1/2 glass of wine back in or around 2000 (during one of my periods of time off of treatment). It made me feel so sick, I decided never again. But, then again, I'm also not SVR and have not ever obtained SVR. I am fairly certain that I was infected back in 1983. I did test positive for non-A/non-B in 1985, but it was at a walk-in clinic and that doctor told me, 'oh is looks like you had some type of old hepatitis infection non-A/non-B in the past and you're over it now'.... No warnings on drinking at all. I don't think that they knew ANYTHING about Hep C at all back then. So, needless to say, I kept on drinking, sometimes have a binge drinking episodes here and there on the weekends w/friends. So, in my mind, this made my virus get more active. Even though I did not have but a mild case of it in the beginning, by the time I was diagnosed in 1994, the process was well under way. If I'd had the ability to know what was going on a lot earlier, (1985), then, I could have stopped drinking then, and perhaps my own immune system would have fought it off. Initially, my liver wasn't in that bad of shape on my 1st biopsy in 1995. But, even after having stopped drinking all these years, my liver still has not improved. Now, I'm up to bridging fibrosis w/no drinking. In hindsight, I wish I had known then, what I know now and I think that I would have stopped drinking a lot earlier.
Susan
Susan
I haven't drank since 1994 (when I was diagnosed), except on ONE occasion when I did try to have 1/2 glass of wine back in or around 2000 (during one of my periods of time off of treatment). It made me feel so sick, I decided never again. But, then again, I'm also not SVR and have not ever obtained SVR. I am fairly certain that I was infected back in 1983. I did test positive for non-A/non-B in 1985, but it was at a walk-in clinic and that doctor told me, 'oh is looks like you had some type of old hepatitis infection non-A/non-B in the past and you're over it now'.... No warnings on drinking at all. I don't think that they knew ANYTHING about Hep C at all back then. So, needless to say, I kept on drinking, sometimes have a binge drinking episodes here and there on the weekends w/friends. So, in my mind, this made my virus get more active. Even though I did not have but a mild case of it in the beginning, by the time I was diagnosed in 1994, the process was well under way. If I'd had the ability to know what was going on a lot earlier, (1985), then, I could have stopped drinking then, and perhaps my own immune system would have fought it off. Initially, my liver wasn't in that bad of shape on my 1st biopsy in 1995. But, even after having stopped drinking all these years, my liver still has not improved. Now, I'm up to bridging fibrosis w/no drinking. In hindsight, I wish I had known then, what I know now and I think that I would have stopped drinking a lot earlier.
Susan
Susan
It might be interesting to poll and see how many do know how they got Hep C. I, for one, have no idea how I became infected.
Personally, I do not feel that alcohol plays any roll in HCV Replication. I do however; think it is FOOLISH to consume alcohol during tx or during HCV. After reaching SVR and determining how low your liver damage is, you have your life back. Do what ever makes you happy.
Frijolie
I have been pondering lately why some of us reach cirrhosis and some of us never get past 1/1. Alcohol seems to play a big factor in replicating the virus and can perhaps account for some of that.
Good question and I have often wandered the same question. But I don’t think alcohol is the Common Denominator. I have had HCV for about 30 years and am a 1-2. I have been a moderate to heavy drinker most of those years. My aunt had it for about 6 years and was a non-drinker. We buried her after an unsuccessful Liver Transplant.
References:
Anand BS, Thornby J. Alcohol has no effect on hepatitis C virus replication: a meta-analysis. Gut. 2005;54(10):1468–1472.
Does Alcohol Use Increase Hepatitis C Virus Replication?
Among patients with hepatitis C, those who drink heavily have more severe liver disease than those who abstain. However, the mechanism by which alcohol use worsens liver disease among these patients is not known. To examine one possible mechanism, researchers performed a meta-analysis of studies that assessed the cross-sectional association between alcohol use and hepatitis C virus replication.
· Three of 9 studies showed significantly higher hepatitis C viral levels in heavy drinkers (defined variably) than in nondrinkers. However, when data from all 9 studies were combined, this difference was no longer significant.
· Hepatitis C viral levels did not increase as alcohol use increased, according to combined data from 4 studies that examined nondrinkers, moderate drinkers, and heavy drinkers. Comments:
This meta-analysis did not find a consistent association between alcohol use and hepatitis C virus replication. The conclusions from this study are limited due to its small sample size, differences in how studies defined heavy drinking, the cross-sectional analyses, and lack of control for the quality of the studies, duration of alcohol use, and antiviral treatment. However, while the mechanism of liver damage from co-occurring hepatitis C and heavy alcohol use remains uncertain, the recommendation for patients with hepatitis C to abstain or minimize alcohol use remains unchanged.
Kevin L. Kraemer, MD, MSc
References:
Frijolie
I have been pondering lately why some of us reach cirrhosis and some of us never get past 1/1. Alcohol seems to play a big factor in replicating the virus and can perhaps account for some of that.
Good question and I have often wandered the same question. But I don’t think alcohol is the Common Denominator. I have had HCV for about 30 years and am a 1-2. I have been a moderate to heavy drinker most of those years. My aunt had it for about 6 years and was a non-drinker. We buried her after an unsuccessful Liver Transplant.
References:
Anand BS, Thornby J. Alcohol has no effect on hepatitis C virus replication: a meta-analysis. Gut. 2005;54(10):1468–1472.
Does Alcohol Use Increase Hepatitis C Virus Replication?
Among patients with hepatitis C, those who drink heavily have more severe liver disease than those who abstain. However, the mechanism by which alcohol use worsens liver disease among these patients is not known. To examine one possible mechanism, researchers performed a meta-analysis of studies that assessed the cross-sectional association between alcohol use and hepatitis C virus replication.
· Three of 9 studies showed significantly higher hepatitis C viral levels in heavy drinkers (defined variably) than in nondrinkers. However, when data from all 9 studies were combined, this difference was no longer significant.
· Hepatitis C viral levels did not increase as alcohol use increased, according to combined data from 4 studies that examined nondrinkers, moderate drinkers, and heavy drinkers. Comments:
This meta-analysis did not find a consistent association between alcohol use and hepatitis C virus replication. The conclusions from this study are limited due to its small sample size, differences in how studies defined heavy drinking, the cross-sectional analyses, and lack of control for the quality of the studies, duration of alcohol use, and antiviral treatment. However, while the mechanism of liver damage from co-occurring hepatitis C and heavy alcohol use remains uncertain, the recommendation for patients with hepatitis C to abstain or minimize alcohol use remains unchanged.
Kevin L. Kraemer, MD, MSc
References:
I have not been drinking any alcohol since 1986 (not a beer or anything) still have high vl 3,8 milj. also relapsed after first tx. But what is exstraodynary is that although I`ve been infected for 35 years no fibroses( st 0). Maybee that has to do with not drinking any alcohol.
My thought is that alcohol can make hcv more aggresiv. I´m geno 3 the most aggresiv form still so little damage so far.
My thought is that alcohol can make hcv more aggresiv. I´m geno 3 the most aggresiv form still so little damage so far.
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