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

[DoubleDose]

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

[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

[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.

[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.

[Undo]

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

[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]

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

[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?  

[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.

[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..

[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]

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.

[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

[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

[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?

[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

[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

[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

[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.

[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?

[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.

[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?

[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!

[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

[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