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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.


27 Responses
86075 tn?1238118691
This is really interesting, and of course a volatile subject...ho hum...that never stopped us...lol....cause on Janis there was this really nice poster we got to know, she was really a nice lady who shared her story with us...she said she was an alcoholic who was told that she needed to wait 6 months for treatment, she did and got sober, etc etc...she was a 1b, did her 48, and SVRed...two years into her SVR, something happened that triggered her off again, and it was off to the races for her and she started slamming back booze again...well after some time of this, she was pronounced positive again! So she treated again, and cleared again...she's been SVr ever since...She swore that even though she was drunk a lot, she was still somewhat lucid, and the thought of hep c scared the cr8p out of her, so she was careful about not going to nail salons, and she never was a big druggie anyway...she got it the first time through transfusion...

she said the docs told her that she must of been drunk and infected herself again, but she swears she didn't...I think we spoke about this before....there was another guy on there that had the same thing happen once he fell of the wagon, and he had a few years of boozing...and he swore he didn't reinfect himself...strange...I mean, I don't know these people and course they could by lying, but I always thought it strange.
223152 tn?1346981971
Interesting article, dd.

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.  I can logically root out reasons why the woman who posted over Janis might reinfect after going off the wagon.  It might be that demon - occult hep C - that was never erradicated and alcohol created a breeding ground for the virons.

However, it is a much harder concept for me to swallow that alcohol use can cause hep C.  I still feel that the virus must have transferred blood to blood.  Assuming there is no IVDU the doors are still wide open for blood transfer.  Alcohol causes aggression in many -- lots of bloody fights, lots of falling and spilling blood .  Probably more bloody intercourse as well.  There are just too many opportunities for not remembering what went on.  Once the little virus enters the body, it would have a wonderous breeding ground.

So my conclusion would be that the alcohol created an environment for hep C replication.  In a healthy individual, the body's own immune system would have taken control and kept it at bay -- perhaps even enough so that an antibody test would not detect it. (I am stretching here...).  But in the alcoholic, that same slight infection would have no chance to become full blown chronic hep C.

It seems to me, most people on our forum, prior alcohlic or not, know from where their hep C came.  
362971 tn?1201990634
Some heavy drinkers also do Cocaine. So they can keep going and drink some more. If this is the case they may not realize that sharing a straw could reinfect them. The nasal passages are very susceptable to infection. and can absorb blood and mucous easily.

388154 tn?1306365291
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.

206807 tn?1331939784
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.

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.

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

Avatar universal
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.
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