Does alcoholism allow HCV to become an active infection???

I am pulling my post on the thread below, titled 'Life Expectance HepC" up to this thread, to initiate conversation around the phenomenon noted in the article cited.  I will also provide a link to the article that Ladybug referenced below.  I find the issue very intriguing and it may, if indeed true, mean that the virus behaves very differently than currently understood.  Here is the post:  (My comments below)

What I find really interesting in this thread is the information in the link posted above on Alcoholism and HCV.  I am going to stay out of the debate on drinking with HCV and drinking even after SVR, because every doctor seems to have a different opinion, and lots of research can be shown to support either case (ie: light social drinking - vs. abstinence).  I don't think we really have a clear cut answer, and since we are all adults, we should read all of the available research and make our own decisions.  I know that I drank moderately for decades before I knew I had HCV.  I stopped completely when I found out, and in fact had almost been abstinent for more than seven years before I found out , since alcohol was affecting me more and more when I did drink.  Now, I have two to four glasses of wine per week on average, almost four years after SVR.  Is it a problem?  Who knows?  I don't think I will ever be able to determine whether this is causing harm or not, compared to total abstinence.  Probably the same could have been said before tx, when I had active HCV.  Alcohol use could lead to certain episodes of abuse, or overdrinking, which then could be very harmful to someone with HCV...etc.  But a drink or two per week????  Who knows.  I don't think you will find a clear answer.

Now here is the issue I am intrigued by, and here is an excerpt from the above linked article on HCV and Alcoholism (linked by LadyBug:

  http://pubs.niaaa.nih.gov/publications/arh25-4/245-254.htm


"In addition to the high incidence of HCV infection in heavy drinkers even in the absence of classic risk factors, other observations suggest that heavy alcohol consumption enhances the ability of the virus to enter and persist in the body. For example, several studies demonstrated a correlation between the presence of virus in the blood (i.e., viremia) and the amount of alcohol patients reported they consumed (i.e., self-reported alcohol consumption, or SRAC) (see figure 2). Furthermore, moderation of alcohol consumption was shown to result in a decrease in the number of virus particles in the blood (i.e., the viral titer) (Cromie et al. 1996). Researchers do not yet fully understand the mechanism through which alcohol affects the viral titer. It is well known, however, that alcohol impairs the function of certain components of the body's immune system (Ince and Wands 1999). An impaired immune function, in turn, may influence the ability of the virus to persist in the body rather than be eliminated by immune cells. "


More than a few references in this long article were made to people 'acquiring' HCV because of alcoholism, in the ABSENCE of normal risk factors...like IVDU, transfusion, etc.

I have read several research studies in the past saying the same thing, and have several times noted that on the forum!  Here is what I think may happen:

Be warned, the following is my theoretical speculation, and is not intended to be interpreted as fact!!!

OK, I think, as I have said in the past, that some or many people may harbor an 'inactive', or 'dormant' version of HCV that is either passed on from birth, or acquired casually, sexually, etc. and does not cause an active, detectable blood liver infection.  Thus, no antibodies on testing, no elevated enzymes, no sign of HCV.  In this subset of the population, those that become alcoholics may allow the virus to move from a 'latent, dormant' phase, into an active infection....the mechanism might be immune system suppression, alcohol's effect on multiplying the virus, or any number of other unknown mechanisms.  The point is that most of these alcoholism studies indicate that alcoholics become (acquire) HCV positive at a much higher rate than the normal population.  And, they are alcoholics who have been weeded out for other risk factors.

All of this fits my theory that HCV can transmit and be harbored by individuals in other ways than the typical active/ chronic/ acute blood liver infection.

For all we know, a major portion of the population could have a dormant HCV virus that would remain unknown, and virtually harmless for life, unless triggered, or activated by something (like heavy alcohol abuse).

I find this subject to be extremely thought provoking, and if you read the research article posted way above in this thread, you will also sense the surprise and curiosity of the researchers who are seeing this data in alcoholics, and trying to figure out why they 'acquire' HCV at such a high rate.  Maybe they already had it, but it was invisible!!!  

So, this is my off the wall thought for the week, and I look forward to the comments it generates.

By the way, if I haven't said it before, I really do believe there is much more about the behavior of this virus that we do not yet understand, than what we do currently understand.  Look at the studies every week implicating a new disease, or manifestation to HCV.  This week, the articles on Diabetes, and the continuing evidence of a link to HCV.

Have a nice day all of you!!!

DoubleDose

[MrsOckert]

I responded on the other thread -

is it the alcohol or is the sugar in alcohol?  Is it true that sugar feeds a virus?  Is excessive alcohol use feeding the virons?

[DoubleDose]

As for 'feeding' the virus, I am fairly certain that the alcohol is more a factor than the sugar, since sugar has not in itself been shown to be a big factor in HCV viral proliferation.  It could also be a factor, but I do not think anyone has singled it out as a problem.

My concern is not about the 'viral proliferation' caused by alcohol, which we are all pretty much aware of already, but the fact that alcohol may in some way play a role, in and of itself, in causing (or activating) the HCV infection itself.  This is the issue that falls out from the studies and data that seems very startling, and confusing.  Why do so many alcoholics acquire HCV, especially those who have NO other risk factors such as injection drugs, transfusions, etc.  Why would alcohol cause someone to become HCV positive?  My theory goes a bit into speculative and uncharted waters, but I think it also explains how something like this could take place.

Just look at the SVR's out there, and those who spontaneously clear.  All the research points to a very low level, non-active, lingering viral presence in these people, many years after clearing.  Well, what about those who never have had the acute or chronic infection to begin with???  Why could they not have or harbor a silent, undetectable, dormant virus that only becomes active after some extreme event?

This is my theory.  I'm sticking to it!

DD

[MrsOckert]

It just seems an enormous jump to say that alcohol causes HCV.  As for having NO other risk factors that just seems like a big jump too.  If someone is indulging in excessive alcohol use (and I've known people who fit the excessive category) most of the time they are indulging in other risky behaviors.  Be it sex, drugs or tattoos and most alcoholics will lie.  Whether they're lieing about the alcohol use or other things.

Just my 2¢ again to keep the discussion open.  I love to hear you talk.

[orphanedhawk]

It is my understanding that alcohol is like an aphrodisiac to HCV. Alcohol consumption  causes the virus to breed rampantly.  If you have HCV then its easy: Coffee- yes, alcohol-no!

[l-horn]

I have no idea where my post went but here is the problem with this 'theory'. One is it relies on 'self reporting' which is not scientific. Two, how do you test for 'dorment virus'. This theory implies that testing for HCV causes HCV. Like Shroedingers cat. Imagine telling your doctor when he tells you you have hepC, 'Well I didn't have it a minute ago...'

LOL....Yeah, sure enough.

This 'theory' requires a little course work in quantum mechanics.

[anise]

Hmmmm, I know of a couple currently serious alcoholics who have hep C and their viral load is very low, always has been.  Their liver biopsies are stage 2.

I also know one who never drank, did drugs, etc.  She got it from a blood transfusion in the early 80's, and her viral load is extremely high.  If your theory is correct the gal who never drank, etc. should be hep c free.  The other alcoholics, which by the way, are only stage 2, both of them, would have seen an increase in their biopsies and VL.

Just my observation.  What are the odds that I would know 3 people who don't fit into the current paradigm?  BTW, these folks came out of the wordwork when I announced I had Hep C 6 years ago.

[DoubleDose]

I am not sure I get what you are saying.  I am not saying that we can test for 'dormant' HCV,... just that it may be there, just like some people can have other dormant viral infections only to see them express themselves later in life, or during a major illness, etc.  HCV is also very good at evading the immune system, becoming invisible, so to speak.  This is why in most cases our own immune system never clears the virus.  It just stops seeing it.  The viral researchers are learning new things about how HCV avoids the wrath of the immune system all the time.  So, what if you were to come in contact with small amounts of HCV in salivary tissues, sexual organs, mucous membranes....rather than from infected blood via IVDU or transfusion.  What's to say that this small amount of virus could not set up a very low level, almost dormant infection in the cells that it comes in contact with?  This is one concrete way the virus could actually be transmitted, or be harbored, without causing a major, blood/  liver infection.  It would also probably not provoke HCV antibody production in the bloodstream, thus would be un-noticed, and undetected.  

I am not sure where you are coming from with your example of someone going to the doctor and saying they didn't have HCV a minute ago, and now do.  Did I say that?  

In these cases, which are documented by a variety of research studies, alcoholics without prior background of any risk factors (IVDU and Transfusion especially) have become HCV positive at a much higher rate than the normal population, and FAR in excess of the normal population that does not have risk factors.  Every research study on alcoholics seems to produce the same results, and the same amazement by the doctors and researchers who conduct them.  They have EXCLUDED former IVDU and others with high risk behaviors from the statistics.  I have provided a possible explanation for this phenomenon.  What is your explanation...other than everybody is a liar?

DD

[DoubleDose]

According to my theory the gal that never drank should INDEED have major HCV infection if she got it from a blood transfusion!  I am not saying alcoholism is how people get HCV infection at all!  I am saying that maybe some of them become HCV+ due to a dormant HCV infection somewhere in their bodies.  Obviously, if someone is an IVDU, or has transfusions, etc. they would be immediately infected if any of the instruments or blood had any HCV contaminated cells.  The way that you generally acquire the HCV chronic blood/liver infection is through contaminated blood to blood transmission.  We all know this.

My question, is: where does the HCV COME FROM in the alcoholics who become HCV+, and who have no prior risk factors?  Read the article, and note the comments of the researchers.  They can't explain it either.

DD

[MrsOckert]

"My concern is not about the 'viral proliferation' caused by alcohol, which we are all pretty much aware of already, but the fact that alcohol may in some way play a role, in and of itself, in causing (or activating) the HCV infection itself.  This is the issue that ....."

Nope, I wasn't following you.  You really are saying what I think you're saying as based on your comment posted above....
"....alcohol may in some way play a role, in and of itself, in causing (or activating) the HCV infection..."

I just have a really hard time with that one.  I'm not the sharpest cheese in Wisconsin, nor am I as bright as many other people on this forum and elsewhere, but aren't there just too many flaws inherent in that statement?

[MrsOckert]

okay, I'm following you now.

My question, is: where does the HCV COME FROM in the alcoholics who become HCV+, and who have no prior risk factors?  Read the article, and note the comments of the researchers.  They can't explain it either.
  
I think that is exactly the point - that there are routes of infection unknown at this time.  I remember the case of the little girl in Florida that became HIV postive several years ago and had NO risk factors known at that time.  I believe they ultimately decided she was infected by her dentist.  

If I'm following correctly you're asking if there are other routes of transmission not currently accepted as status quo and whether drinking heavy amounts of alcohol awakens the so-called sleeping dragon after many years of indulging?

[l-horn]

" What is your explanation...other than everybody is a liar? "

[DoubleDose]

No, you were right the first time.  I am more saying that the alcoholism 'activated' a hidden, or dormant virus.  Not really saying that it 'causes' the virus to exist, but that it may prompt it to become a real infection, from a previously dormant or inactive state.  Where we may pick up this 'dormant' version of the virus would be anyone's guess.  How many in the population might have a 'dormant' version of the virus is also up for grabs.  BUT, I do believe there are other transmission routes, AND other modes of infection.  I think that a dormant HCV infection could be in cells or organs, and never get into the bloodstream at all, unless prompted by something like major alcohol abuse, immune system shutdown, major catastrophic illness, etc.  

No, I am not quite as nutty as you were beginning to believe.  I don't think alcohol creates HCV, just paves the way for it to blossom, in those who might have a hidden or dormant infection.

I even suspect that parents in prior generations might have passed this dormant infection to children, and they might in rare cases one day become HCV+, never knowing how they acquired it.  There are many of those cases out there, by the way.  A great number of people really don't have any idea how they got the virus, and have no real prior risk factors.  

The fact that many drug users come down with HCV is no surprise, because they are injecting infected blood from person to person.  This group is outside the profile we are discussing, as are transfusion cases.  Direct blood infection causes the active HCV infection, without any doubt.

I am more concerned with another mode of infection, and hence by necessity, another mode (or modes) of transmission

For doctors and researchers that routinely find HCV virions in gastric fluids, saliva, sexual fluids, mucous membranes, lymphatic system (though it is not always there, it is often harvested), I wonder what they think happens to this virus when it is exchanged with fluids in other close contacts (kissing, sex, sharing foods, etc).  Does it just 'wash right out' of their systems?  Does it reproduce a little bit and then say goodbye?  Or, might it not set up a localized cellular infection, remaining under the 'radar' for many years, or for a lifetime?

One of the major Hepatologists is beginning a research study this year to study just this question. The focus is on family members and close contacts of HCV infected persons, to determine if there are cellular immune responses to HCV in their fluids, organs, etc....even though they are negative for HCV on antibody tests, and PCR tests.  I imagine what they are looking for is just what I am speculating about.  Are there local areas of cellular HCV infection in those who are close or intimate contacts of HCV + persons?

It will be very interesting to see where this study goes!

DoubleDose

[DoubleDose]

Re-read my post above, and see the reason.  Alcoholics may just be activating an already existing, but dormant, and undetected HCV virus.  In a nutshell, that is what I am saying.  Those  non-alcoholics out there who might harbor this dormant virus probably never will provoke it to cross the blood or immune system barriers, and become a real HCV blood infection.  Thus the alcoholic population has a vastly higher HCV infection rate, because alcohol is the 'catalyst' in triggering the latent virus.

DD

[anise]

My point had to do with viral replication and alcohol.  I hear this a lot and not totally convinced that alcohol replicates or causes the virus.  

As for your theory, I tend to go along with MrsOckert - I took that you meant alcohol causes or activates HCV.   I also believe that alcoholics are adverse to telling the truth.  They have so much shame to begin with, why would they put further shame on themselves?  Thus, the disconnect behind alcoholics, doctors and researchers.  Again, just my opinion.  

[anise]

Didn't read your most recent post.  I do understand you mean 'activating' the virus through alcohol.

[GrandmaA]

I was not an alcoholic. I had antibodies for hep. C. (all my liver studies were normal). I was in the acute phase. I did not get the chornic illness until I took 1 1/12 bottles of kava kava. People with hep. C can NEVER take it.

[Forseegood]

I had posted this before a while before and got roundly thrashed...this is a more civil board now, in my view, so maybe I'll only get a mild thumping, lol....on Janis, there are a few posters who have reported this...of course, this is purely anecdotal and non-scientific, though I just thought it interesting...

I really don't believe that either of these posters had any reason to lie, they seemed like nice people and had been posting there a long time, one of them still posts...it's up to the other members who know them (as well as you can know anybody on a board) whether they want to actually *believe* them or not...

One was a woman from Atlanta, who said she had a very bad alcohol addiction, but when she found out she had this, she said it got her *scared sober* and she even decided to do treatment...I'll call her Mary...well, after 48 weeks she SVRed and was very happy,...after about a year and half, or maybe two, she started drinking again....heavily....

she came down with the virus again...people on the board (and her doctors of course) questioned her and asked if she possibly got re-infected, and she said, even though she was drunk, she was still paranoid of this virus (after having done treatment especially) and was living by herself...she *said* she did not shoot-up or do drugs, just alcohol...

well, she did treatment again, and SVRed again, and has stayed sober saying she's going to not be some knothead again...there was another male member there that had kind of the same story, though the details were a little differently naturally...both people said they had began to drink "heavily" not socially, which should be stated...

the male said that he was going to do treatment again cause he had SVRed before, but they haven't heard from him again as far as I know...

They both said that their doctors were very interested in them because of their stories.......but really hadn't followed anything up, and in the end their doctors just figured both had re-infected themselves while drinking...

Of course, I know of more then a few people who drink occasionally who have SVRed and they seem fine...like I said, I just thought this interesting, but of course, there is no way of proving any of it...

[MrsOckert]

I certainly hope this is a more civil board.  I see no reason why your post should produce any "thumping".

It certainly would go along with DD's theory about activating a dormant virus.  I'm still not convinced that SVR for 5 years means "cured", but please don't anyone thump me.

DD keep us informed of these studies - this is a very interesting topic.

In the same vein, but different .....

Some people say you absolutely cannot get HCV from sex and use the anecdote that one has been married to the same partner for 35 years and the partner is clear.

But don't they say that your risk of STD's increases with the amount of partners you have/had?

Let's say someone had five partners in their life and HCV is not easily transmitted via that route.

But what if that same person had 200 partners in their lifetime and 20 of those partners were infected with Hep C - would that person's chances for contracting it that way increase?

And if it would but was so miniscule as to not cause a full  blown virus attack could drinking large quantities of alcohol over a number of years exacerbate an attack?

[DoubleDose]

Thanks for your comments.  I think I remember your bringing these cases to our attantion in the past.  Of course everyone is so locked into whatever the current thinking says, that in many cases they just don't want to look beyond the commonly held assumprions, and find a potentially deeper understanding of the virus. Maybe its fear, maybe its pollyanna thinking, I don't know.

The re-activation issue, after SVR, has already been written about in the several cases of heavy immuno-suppression drugs given to a few foormer HCV+ / long term SVR individuals, who were about 7 or 8 years SVR.  Everyone wants to assume the stories must be incorrect, or that they were re-infected by HCV through some other risky behavior, etc.  I think the virus just re-activated because the immune system was unable to keep it in remission.  I think the 'remission' concept is coming closer to being either proven, or just quietly acknowledged by the medical and research community.  

More than ever the researchers seem to think that some form of HCV remains, longterm, after SVR, and some of the doctors are couching their language regarding 'eradication' to include this possibility.  So, though they may say 'cure', they mean it with a small 'c', and mean the virus is probably not going to return, but not that it is totally eradicated.

So, I say, if the virus can still be 'there', in SVR's, and in those who spontaneously cleared, then why not also in people who have never gotten the chronic blood/ liver infection?????

Many of these people may have come in contact with the virus in some form, and are keeping it in-check just like the SVR's do.  The only difference, is that have not gone through actually having an active blood HCV infection, and hence will not test positive for the virus on blood testing, etc.
The 'dormant' or 'hiding' virus may in fact be undetectable, or only seen on extremely high amplification, or on cellular tissue testing.

So this idea can easily explain why alcoholics might have a far higher incidence of HCV, without shooting drugs, or any other risky behaviors.  They may just be letting their immune system barriers all the way down, and allowing a very dormant, unseen virus explode into a real, and chronic HCV blood infection.

The stories you relate, about several SVR's going back to heavy alcohol abuse, and becoming HCV positive again would fit this theory perfectly!  I think there should be much more study of these sorts of cases when they occur, and doctors should not be so quick to automatically and reflexively  find everyone 'guilty' of reinfecting themselves, just because it fits 'their own' existing theories about HCV.  Especially when the persons who become HCV+ again show no real probability at all of having risky behaviors, and are adament that they did nothing to reinfect themselves.  Very few SVR's would ever be so stupid as to do a high risk behavior after having the discipline and courage to withstand therapy and become virus free.  Especially those who were never drug users to begin with.

I clearly believe that the virus may be acting in ways yet to be understood or explained by current medecine, and the data seems to be demonstrating that the thinking needs to change, rather than trying to force the standard thinking onto the facts.

Thanks again for your info!!

DoubleDose

[cruelworld]

i may have missed the whole point of this thread but this might be helpful. ive recently read everything i could find about alcohol, HCV and immunosupression.
its fairly well understood. google it. on the one hand alcohol does overwork the liver and chemically fuel an existing hep c fire to multiply the damage at the liver site.. but its real danger in disease aquisition and relapse is its immunosupressive quality. i beleive this explains most everything.
alcoholics have to fight all sorts of other diseases they would have never gotten
if they had not been immunosupressed. we, as heppers (who must always carry a trace of the virus) must be acutely aware and overvigilant to never do anything
to suppress our bodies fighting mechanism. i beleive even simple things like lack of sleep and or poor diet can be asking for trouble. to stay well, (no relapse) keep your immune system top notch.
alcoholism and hcv
http://www.medscape.com/viewarticle/488940_2
you will have to register or log in, but its free and a great study

[anise]

I see your point, both of you.  

Something my Chinese doctor told me has me thinking - is that we can live side by side with the disease.  His herbs boost the immune system, (btw, he claims several folks under his care have became UND).   So as long as you keep the immune system healthy you have subdued the virus.  Sounds like we really don't need treatment but tend to healthy ways, such as, eating, keeping in shape and positive thinking.  What a way to go, love it!

[Forseegood]

Even though this is about HIV, it does talk a lot about *immune response* and a virus...I don't know how much we can extrapolate from this article, but maybe the more *scientifically inclined* among us can take a shot...or anybody for that matter, he he...



AIDS drug cocktails may be able to restore the ravaged immune systems of some people infected with HIV, researchers reported on Wednesday.

Immune cells known as CD4 T-cells returned to normal levels in an ideal group of patients, picked because they responded optimally to a combination of at least three AIDS drugs, the researchers reported in the Lancet medical journal.

The human immunodeficiency virus, which causes AIDS, plunders the immune system, leaving people vulnerable to a range of infections that may prove fatal.

AIDS is incurable, but doctors try to prop up the immune system with life-extending drug therapy aimed at reducing the amount of virus in the body.

The study involved 1,835 HIV-infected people drawn from a larger study involving more than 14,000 patients from across Europe, Israel and Argentina.

"I think it's very encouraging that if people can respond to treatment well enough and can suppress the virus for long enough, we have sufficient evidence to say their CD4 counts can return to normal," Dr. Amanda .... Medical School in London, one of the researchers, said in a telephone interview.

"Our previous understanding was that there was a plateau in CD4 counts so that CD4 counts would stop increasing after a sufficiently long time taking combination therapy," she added.

Dr. ......said not all HIV patients respond as well to these drugs, and many, particularly in the hardest hit regions like sub-Saharan Africa, do not have access to them.

"This is sort of the best-case scenario, if you like, that we can identify a group of patients who we would expect to have a normal CD4 count with sufficient treatment," DR.....said.

These patients were chosen because they responded well to the treatment, with the drugs suppressing the virus to very low levels. They were tracked for about five years.

Dr. Anthony director of the U.S. National Institute  and Infectious Diseases, said doctors who care for HIV-infected patients have noticed this restoration of normal levels of CD4 cells in some of them. DR. credited DR.s team for documenting this phenomenon in a systematic way.

CD4 cells, a type of white blood cell, help protect the body

from infection. But HIV targets CD4 cells, using them to create

more copies of the virus, thus undermining the immune system.

After initial infection, a person can produce more CD4 cells to take the place of those attacked by HIV. But in time, the body cannot make enough, increasingly weakening the immune system.

Although it is impossible to eradicate the virus with existing drugs, it is possible to keep it at extremely low levels in some people with the right combination of drugs.

The AIDS virus infects close to 40 million people globally, most of them in Africa. It has killed more than 25 million.

[DoubleDose]

I agree with everything you said, though many on the board might disagree with you.  I think the idea that after SVR we could relapse from extreme behaviors has not yet been very much accepted.  Many still resist the idea that there is a lingering latent virus being held at bay, but unfortunately I believe that is the truth.  I am also concerned that this persistent, low level infection is also causing some of the long term problems we experience as SVR's.  Maybe our immune systems are in a perpetual state of overactivation, in dealing with the now-contained, repressed virus, or maybe the low level virus itself still causes malfunctions in system and organ function, etc.

I have yet to meet many (if any) SVR's that really feel like a million dollars...or feel like they did prior to HCV infection.

The out-of-the-ordinary part of my speculation above, is not the part about re-activating the virus with alcohol after SVR, which I think some people already believe is a possibility, but I also think the 'inactive, low level, or undetected latent virus might be found in many people out there who have never come down with a true HCV infection.  Kind of like an SVR without ever having had the disease or treatment.  Just the low-level, undetectable virus, being held in check by the immune system.  Hence, the alcoholic population experiences a high level of viral breakthrough, into a full blown HCV infection.

Thanks for the input.

DD

[DoubleDose]

Oh I think we definitely need treatment IF we have the active blood/liver virus.  This is fully detectable, and easily diagnosed, along with liver damage, andviral load.  This is the full blown infection, and is just what does really need treatment.

We are talking about the virus-in-remission...whether in SVR's, spontaneous clearers, or MAYBE, as I have suggested, in many people without any hint of the HCV disease, and without antibodies.  

DD

[copyman]

you have been posting very interesting 'theories" lately. i have agreed with at least one about the sinus/throat infections but disagree with this one. you must have a lot of time on your hands to come up with this stuff :-) not sure if this is really helping anyone and perhaps should be posted on the other side. you have a vast knowledge of HCV and people here would benefit much more if you could help with a specific answer to a question instead of these "theories". of course just my opinion.

[DoubleDose]

This theoretical stuff regarding  the prevalance of HCV in alcoholics is the result of trying to come up with sensible explanations for the extremely high rate of HCV infection, per the above article, in the non-IVDU alcoholic population.  I don't think that it is very far off  from the 'persistent virus after SVR' facts that have been publicized by numerous research groups in the past few years.  

DD

[cruelworld]

i personally believe that dormant hcv is probably greatly spread thoughout the population. 20% to 50% of everyone could already have at least one hcv viron in their system. take the herpes facial virus, 60% of the population have it!. same situation.
it may very well be that spittle has a few undetectable hcv virons in it. easily spread, one viron at a time. there are also many other latent viruses in large percentages that humans harbor and may never see. the immune system keeps them down so long as its strong. immunosupress and they start popping up. i intuitively wouldnt put as much weight on the theory on that the tiny sub level infection causes problems. but i do put weight on it and hope they
study it more. keep the info comin double dose.

[grammajen]

This is an interesting discussion.  

A little personal background to my comments:  I had just moved across the country and started seeing a new family doctor that did not know me or my history for the past 26 years (as a nice church lady who didn't drink).  When she was screening me for an ovarian cyst operation the routine blood tests showed a high AST and ALT and she asked why they were so high--did I drink?  I would have an occasional glass of wine with a meal but it was not daily, weekly, or even monthly.  She asked again, Are you sure you don't drink?.  The doctor wrote on my chart, "patient denies active use of alcohol".  I suspect she did not believe me.  During our discussion I remembered that my first husband whom I had been married to until 1980 had been diagnosed around 1996 with Hep C.  So maybe that is why my ALT and AST were elevated.

So I don't drink but had elevated AST and ALT that eventually the doctors decided was caused by the Hep C virus.  

Now, one of my siblings was tested after I was diagnosed and she had also been exposed to Hep C but she was one of the people who cleared the virus on her own and developed antibodies to the virus.  Now this sibling is a 40 ounce a day white rum or wine drinker.  I told this sibling that maybe I should have been drinking all these years instead of babying my liver with healthy living :)

[honey11]

I just don't get it either!  I had hep c for probably 25 years and my husband also,,,,,Were we drinkers during those years??  Noooo,,,,nothing,,,,a very occasional drink on a holiday or so but you would never find any liquor at our house to drink.  When I was tested positive for hep,,,my viral load was 8,5 mil.   My husbands was 600,000 so on one end very high viral load and other end,,,low.  I have also read many articles that lots of people with hep c have past drug,,,and alcohol issues???  Could this mean that lots of people that do indeed have it,,,,also have addictive lifestyles so if it isn't alcohol,,,,,could be drug issue??  I'm not sure but I really don't feel that alcohol can revive hep c but I do believe its not good for the liver so if you choose to drink after you have reached SVR and after you went through tx for 6 months to a year,,,,,that we all know,,,,,,it could be doing more possible damage to your liver which needs a break after the disease!

[DoubleDose]

How did you and your husband contract HCV to begin with?  Do you both have a pretty solid idea of when and how it happened?  

DD

[DoubleDose]

Your story is a scary one!  Do you believe that you were infected prior to 1980 by your husband, but maybe never had any clinical signs of the virus, or do you believe the virus manifested itself much later, sort of in a delayed manner, in your case.  It seems you did nothing to trigger it if it had indeed been a 'latent' infection.  Possibly you were infected early on by your ex-husband, and never had any obvious clinical abnormalities.  Did you ever have HCV antibody testing done, prior to your doctor's discovery of the elevated LFT's?  Did you and your prior husband ever share in any blood related interactions....during surgeries, illnesses, being cut, etc???  How do you explain the transmission of the virus to you?

DoubleDose

[honey11]

Hi DD,,,we thought we knew all this time that it was related to an automobile accident and my husband had to receive blood in early 80's and that I caught from him but past year now,,,,we are having our doubts and not sure.  We are thinking it could be an earlier incident where we did do some drugs at a party and the reason I 'm saying this is because,,,,2 people that were close friends at the time and at this certain party contacted us just this past year and asked if we had hep c???  We were shocked and said yes,,,treated and cleared and they said they had also,,,one with cirrohsis and failed tx twice and other never treated and didn't want to so that was a real shocker to both of us to get this phone call but now,,,it all makes sense!
I'm looking for your thread on sides from hep!  Very interesting and I wrote a long post yesterday and hit sent and it didn't take,,,,lol    Geeze so got off computer but interesting stuff,,,,and I will find this evening!   Glad to see you still here and participating in all the mysteries of hep!

[pigeonca]

Here's a question: Do immunosuppressive drugs activate the hcv virus after SVR?  I know that we need to be careful about steroids, and my dermatologist wants me to avoid, at least for now, such things as methotrexate and UV light therapy because they mess with the immune system.  If alcohol in large doses causes relapse, then wouldn't these drugs and therapies do the same?  In the same vein, I know people like Mike Simon have achieved SVR after liver transplants?  Don't they have to take immunosuppresants for the rest of their lives?  If so, why don't they relapse?

[cruelworld]

remember, mike simon (details may be inaccurate) had a relapse soon after end of treatment and the pcr caught it
at  viral load  50 or something low, his own immune system suppressed it fairly quickly and he is still svr.
hard to argue that one.

[GoofyDad]

From way up there: "Alcohol consumption  causes the virus to breed rampantly. "

Not suprising, as it's had a similar affect on myself. I  wonder whether the virus selectively targets fat chicks with badly dyed hair, as that was my usual point of entry.

------------------------------------------------------------------------------------------------
On a more serious note - I'm pretty convinced that SVRs still harbor viable virus down in there somewhere.... but at this point I'm not too excited about it. An interesting question is whether one can be exposed and be a 'silent carrier' of HCV without showing antibodies. Or can one be exposed and repell the virus without developing detectable antibodies?

[pigeonca]

I imagine both might be true regarding exposure without showing or developing antibodies. especially if the virus is passed on at birth.  I've even wondered if my grandmother, who had cirrhosis despite being a non-drinker (except for Manischevitz on holidays - she was a rabbi's wife), might have had hcv, passed it on to my mom, who passed it on to me.  They're both gone now, so testing isn't possible, but it could be.

[CockSparrow]

If your theory were true, there would be a lot more relapses after SVR than there currently are.
I doubt alcohol of and by itself activates HCV.
The sugar concept is somwhat interesting, as its carbs that contribute to Fatty Liver.
HCV + Alcohol = HVL and poorer response to Tx so maybe something in the alcohol/carbs as hcv food.
CS

[DoubleDose]

My mother also died with a syndrome much like liver failure, along with a major stroke.  She had suffered fatigue for about twenty years, had skin problems, joint aches, thyroid issues, and later water retention and jaundice.....sound familiar????

I often wonder whether she had this throughout her life.  No testing twenty years ago,  Oh, AND she had elevated LFT's...which the doctors said were from heart problems!!!  I even wondered back then!

DD

[DoubleDose]

No, I don't think there would be more relapses.  I think the 'latent' virus stays just that way, unless a 'major' event triggers its activation.  Most people would remain 'latent' just as the SVR's seem to remain 'undetected' for the active infection.  I would think this same 'latent' virus exists (in the SVR's and others also), and only heavy binge drinking, or major immuno-suppressive drug therapy, or crisis illness might reactivate it.

Much of the population that carried this 'latent' form of the virus would continue to 'fly under the radar', and would never be detected by standard testing .

DD

[beamishboy]

interesting thread..i wonder about other mitigating factors as well..alcoholism often accompanied with v poor diet ,sleeping patterns and such..pre-existing psychological impairmnts and neurosis' may also affect the immune system..To wit: depression,mania,poor self-image..might not all these factors undermine our immune systems? i believe mental health and sanguine equillibrium are also important for physical health...Regular active physical activities also..How healthy can a heavy drinker be,given all the subsequent and underlying self destructive behaviors?

[mikesimon]

I didn't relapse, if by relapse you mean that I became serum detectable - that is the accepted definition of "relapse" to my knowledge. I have not been serum detectable per Heptimax <5 IU/ml since April 2003 and I test every month. I had a biopsy in June 2006 after a major dose reduction in my anti rejection dose and a small amount of HCV was detected in the biopsy sample: 30 IU/ml. It was my surgeon's opinion that the dose reduction stimulated my immune system which then began to attempt to eradicate the little bit of HCV in my liver which caused an elevation in my enzymes. I believe my surgeon to be a brilliant physician but I am not convinced that actually was the case and I still entertain the possibility that I was experiencing acute organ rejection due to the dose reduction. However, my surgeon also told me that he has seen transplant recipients clear every trace of HCV  and then have organ rejection issues. His line was "maybe a little HCV is  good  for you". The obvious suggestion was that once the immune system is unburdened with watching or controlling a trace amount of  HCV it might start to attack the liver. How this fits into the theories expressed here and the overall discussion is beyond me. Mike

[CockSparrow]

If what you say were true then patients undergoing certain drug Tx or chemo would develop higher relapse rates. This has occurred on rare occasions btw. What i mean by this is if your theory is correct there would be pockets of higher HCV relapse in these groups. Possible i guess, but nothing indicates it.
All sounds a bit like occult HCV to me.
CS

[willing]

sure looks like blood isn't:

First case of hepatitis C virus transmission by a red blood cell concentrate after introduction of nucleic acid amplification technique screening in Germany: a comparative study with various assays.
Vox Sang. 2007 May;92(4):297-301.
PMID: 17456153 [PubMed - indexed for MEDLINE]

From their conclusions:
"In summary, we have shown that hepatitis C infection was acquired by red blood cells from a blood donation tested negative for HCV RNA by a highly sensitive routine NAT assay. To our knowledge, this is the first case of a low-viraemic red blood cell concentrate from a pre-seroconversion donation infecting a recipient since the introduction of mandatory NAT screening in Germany in 1999. Thus, a very small infectious dose apparently resulted in an HCV infection. In this case, even routine screening with individual donation nucleic acid techniques, which are the current state of the art in this field, would not have prevented this case of hepatitis C transmission "

the donor showed UND on pretty much all the standard commercial tests. Versant's TMA, which Jim is fond of, struck out 5/5. The only commercial test that came through   with flying colors was Cobas TaqScreen MPX .

Body fluids on the other hand *may* be safe, possibly  an important point in the pre-foreplay negotiations.

[jmjm530]

Willing: the donor showed UND on pretty much all the standard commercial tests. Versant's TMA, which Jim is fond of, struck out 5/5.
----------------------------------------------------------------------

How did your fav 50 IU/ml PCR do:) Hopefully, newer papers/presentations, including the Berg article,  -- or partial translations here -- have persuaded you that the more sensitive tests -- possibly not perfect -- do have clinical utility in treatment.

But seriously, the Versant TMA and it's Quest version (HCV RNA QUAL TMA -- sensitivity 5 IU/ml) are well accepted tests and I got it from a pretty leading fellow in the field who preferred it over Heptimax, which I don't believe uses the Versant method although has the same sensitivity (5 IU/ml). Can you post a link to or exerpt he rest of the study where it critiques the different test formats, although it appears that the study wasn't set up to conclusively test one TMA against another, but for other purposes.

-- Jim

-- Jim

[willing]

I'm just on my way to the airport but will see if I can find a place to park the results when I get back in a week. The relevant stats are in tables 1 and 2. Yes, they didn't really set out to do a comparison, just wanted to show that the chances of this guy getting detected on any commercially-available test were very slim. And no, I didn't look at the less-sensitive tests but I'm sure you're right about their  faring no better..

[GrandmaA]

I know a lady who was genotype 1a and she cleared the virus with tx. But she also had lupus and one of her doctor's gave her prednisone and the hepatitis C came back - relapse. She had to go through tx all over again.

[GoofyDad]

willing: Body fluids on the other hand *may* be safe, possibly  an important point in the pre-foreplay negotiations.

So what do you propose, she should switch hands just before the moment of glory?  

[Undo]

I have to admit, thats pretty goofy.   Or maybe NOT.     I'll keep you posted.  LOL

[willing]

goof: may not be safe enough. I was thinking, thick, all-body,  latex with a hermetic seal. Kind of a diving suit, but in romantic colors.

jim: OK here's that table:
-------
Table 1 Qualitative analysis of HCV window-period donation (genotype 2b). Donor plasma from the window-period donation was subjected to various qualitative and quantitative assays. In each assay, the samples were tested in five replicates. The characteristics of the assays are indicated

Assays Technique Sample volume preparation/equivalent (ml) a LOD b (IU/ml) Results (HCV RNA reactive/total)

Qualitative CE marked for blood screening
  Procleix HIV-1/HCV assay TMA 0·5/0·5   1·9 0/5
  Procleix Ultrio assay TMA 0·5/0·5   2·8 2/5
  Cobas AmpliScreen HCV test, version 2·0, MultiPrep PCR 1/0·25  28·8 1/5
  Cobas TaqScreen MPX Test Real-time PCR 0·85/0·65  10·7 5/5

Qualitative not CE marked for blood screening
  Cobas Amplicor HCV test, version 2·0 PCR 0·2/0·05  43 1/5
  Cobas AmpliPrep/Cobas Amplicor HCV test, version 2·0 PCR 0·5/0·33  10 3/5
  Versant HCV RNA qualitative assay TMA 0·5/0·5   9·6 0/5

Quantitative CE marked for HCV RNA quantification
  HPS/Cobas TaqMan HCV test Real-time PCR 0·5/0·33   9·7 3/5
  Cobas AmpliPrep/Cobas TaqMan HCV test Real-time PCR 0·85/0·65  12·6 3/5
  Abbott RealTime HCV assay Real-time PCR 0·5/0·28  10·5 4/5
  Amplicor HCV Monitor, version 2·0 PCR 0·1/0·005 600 0/5
  Cobas Amplicor HCV Monitor, version 2·0 PCR 0·1/0·005 600 0/5

a Sample volumes for preparation and the corresponding plasma equivalent for amplification/detection are indicated.
b LOD, limit of detection: 95% cut-off according to package insert (WHO standard genotype 1a).  

TMA, transcription-medicated amplification; PCR, polymerase chain reaction; HPS, High Pure System.
----------
I tried to fix the formatting a bit, but it's still a bit hard to read. There are 5 columns, the last being the number of detections out of the five assays done. Note that the 3 TMA-based tests scored 0/5, 2/5 and 0/5  whereas real-time-PCR-based scored  5/5, 3/5,3/5 and 4/5 suggesting that's the more reliable technique. The 5/5 was the "Cobas TaqScreen MPX".

I believe the most common  PCR-based test (with LOD 50 IU) is the Cobas Amplicor v2 and, as you anticipated, it also did poorly (1/5).

"CE marked" refers to  EU regulatory approval and shouldn't be relevant here.

[Undo]

dont forget the resevoir tip, for the discerning snuff dipper.

[jmjm530]

Thanks for the tables. I've heard similar about PCR's being more reliable than TMAs, at least in terms of false positives -- however, here we're talking false negatives. I also thought the Bdna (sensitivity 600 IU/ml) had the most accuracy within its limits.

[ladywhy]

In 1991, I got sober, a year later was dx with Hep C. Tried straight interferon, then when the clinical trials began..what in 93? I did riba and interferon. I was considered acute when dx. No liver damage..don't know the vl. Anyway...i was very ignorant and UND was SVR to me. Stopped seeing dr.s and went to alternative meds/accupuncure etc.. to get stronger. Then after 9 yrs. of sobriety..I relapsed and had no tolerance for alcohol...though that didn't stop me from drinking. By the grace of God, I have no desire for it...but it does make me wonder if by my drinking..I did reactivate it. I do believe that may very well be true in my case. I say reactivate as I did dabble in IVDU for a very short time and I did have a blood transfusion in the early 80's. That's my shameful story...it 'aint pretty but it is true.

[meki]

It was the Darn Twinkies I'm telling you.

Twinkies... they did it... Sigh... I knew it.

OK - I fall out of every category... Except for surgeries, dental work and a shot of gamma globulin (rhogam). Those are the only ways I could have contracted HCV.

Why?

Because I never did needles.... The Tattoo I have was done with a single usage needle that was taken out of the package when used on me --- in a brand new bottle of ink. I didn't have unprotected sex except for during my marriage. I didn't needle stick myself during any of my EMT days, nor did I share razors or toothbrushes with anyone (I think I'd rather have been strung out on needle drugs than share a toothbrush.... LMAO!)

I don't drink very often (now or then) - and I never hung around people who (knowingly) were IDUs or had any known diseases. (Not that I wouldn't hang around people who were doing that or used to do that or had any diseases... I just never knew anyone who did.)

Also --- for the US I have/had 3a... So that, in itself is a bit unusual. Yanno?

So it had to be the Twinkies.

LMAO!

On a serious note: I was wondering if perhaps Mrs. Ockert hasn't hit on something very interesting.

SUGAR. Is it the breakdown of the sugar that excaberates the HCV into becoming active, when it is leading a semi dormant lifestyle.

AND if so - does the pancreas play a role in keeping it dormant --- until when we all get a bit older, the pancreas becomes more tired... and stops keeping it under control. Regulating it?

That's a good conversation in my book.

Hugs to everyone - and may you all have a sunshiney day - no matter where you are --- or what the weather is like.

Meki