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Post Info TOPIC: Can hep c live in the liver, macrophages or lymphocytes after SVR?


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RE: Can hep c live in the liver, macrophages or lymphocytes after SVR?
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Love a good copyright infringement brawl (and plagiarization)! My favs! 

I liked the one Linux coined, "C-Begone", hee-heee, AND mine, borrowed from a brylcream commercial " a litle dab will do ya" ("dab" that's what they should call these short courses of sof/vel/vox)! Sheesh, what should a one day/one dose course of RG101 be called?! confuse

This is all Pablo and Skewed's fault!, THEY started it! smile C. 



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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I didn't want to "read" that online Wiley stuff, but didn't have the common sense to stay away. I used those quotation marks because when you don't understand more than 30% of words in any given sentence, it's probably not what youre doing. But I did get the bit about the virus still being detectable after nine years in most guinea pigs. That made me sad until I read Pablo's take on it. And  yes, once a zap was added I knew Dave's tin foil hat, Jimmy's  I'll take that thanks and look here's what it goes with stuff and Tig's wry commentary would all come rolling in. 

Predictable = funny = safe.

What would we do without you all? 

Syd 



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Contracted Hep C 1969. Genome Type 2, treatment naive. Began 12 week RIBA/sof/Dac on 12/11/15. Cirrhosis. VL before treatment 4m. Treatment extended another 12 weeks without Riba. No virus detected at 9 weeks.



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Maybe we should apply for a trade mark?



-- Edited by Pablito on Sunday 3rd of July 2016 07:07:10 PM

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44 y.o. male, HCV G4 since 1996, F-scan score 9, F2, Failed prior I/R, finished sof/vel/vox 8 weeks 5/16, pre-treatment VL 2 million, EOT UND, EOT+4 UND, EOT+12 UND.



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Good thing you live by the sea.



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Harvoni TX 2 12 weeks. UND weeks 4, 12 and now EOT + 4 Weeks. SVR-12 09/29/16. All Glory, Honor and Thanks be to God.

"I go to war with the brothers I trust."

Tig


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ZAP THE MAGIC DRAGON, LIVES INSIDE OF ME......   We need a musical rendition of this, you know the theme I'm thinking about! biggrin



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Tig

67yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 9+ years!

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LOL, I knew that with ZAP in the picture it wouldn't take long for Jimmy to chime in.

Zap would be a great name for it though. Ads would say "Zap the Dragon" ... as a big bolt of lightning strikes the beast.

... don't know about you but I'm wearin' my tinfoil hat if I take it.

 

D

 



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63yy,HCV,2b,F3-A1, Sof/Riba,12wks Tx   SOT: 1/20/16, HCV-RNA 9,816,581, ALT 56, Hb 14.6

4wk: HCV-RNA <15 Detected, ALT 15, AST 17, Hb 13.6 EOT: 4/12/16, ALT 18 , Hb 12.9176a2f85d05d9c965eafe199f2ba9ba5.jpg SVR Achieved 7/8/16

 



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I remember reading a few years back that there were pockets in liver damage where particles could hide out and slowly reproduce. But I also read the particles were not able to reproduce in some people and others they were - a bit like "brexit" the opinions were divided.

Now they are calling it a cure, because we are stopping the reproduction of the virus, so I actually believe in most cases it will be a complete cure. The human body is full of viruses like Chicken pox. The immune system controls and contains it, but in a rare few they develop Shingles. Why only some, nobody knows. It can be a very weakened immune system and some particles reactivate. Either way, most doctors now consider us NOT infectious although they wouldn't take a blood donation from us. 

Since we are blocking, rather than destroying, it can't reproduce so its bye bye from them :D



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Genotype: 3b

VL.�over 15, 000 000

Failed TX 2014: Interferon/Riba.

Cured using Sof/Dak combination.

I can eat cake again! <3 



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Tig56 wrote:

That ZAP stuff, that's the ticket! At least we have a name for it when it's developed... biggrin


 Copyright Infringement!

Zap! has been around since 1968. biggrin



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Harvoni TX 2 12 weeks. UND weeks 4, 12 and now EOT + 4 Weeks. SVR-12 09/29/16. All Glory, Honor and Thanks be to God.

"I go to war with the brothers I trust."



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Pablito wrote:

Jimmy - 

In 2020 Jed goes to his hepatologist, and he is prescribed a 3-day course of sof-vel-vox-dac-zap.  And he's cured.


 LOL no doubt. That was good!

 

 

JimmyK



-- Edited by JimmyK on Friday 1st of July 2016 07:40:14 AM

__________________

Harvoni TX 2 12 weeks. UND weeks 4, 12 and now EOT + 4 Weeks. SVR-12 09/29/16. All Glory, Honor and Thanks be to God.

"I go to war with the brothers I trust."

Tig


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That ZAP stuff, that's the ticket! At least we have a name for it when it's developed... biggrin



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Tig

67yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 9+ years!

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Jimmy - 

In 2020 Jed goes to his hepatologist, and he is prescribed a 3-day course of sof-vel-vox-dac-zap.  And he's cured.



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44 y.o. male, HCV G4 since 1996, F-scan score 9, F2, Failed prior I/R, finished sof/vel/vox 8 weeks 5/16, pre-treatment VL 2 million, EOT UND, EOT+4 UND, EOT+12 UND.

Tig


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Based on the article:

"This continuous presence of HCV RNA could explain the phenomenon of relatively common persistence of humoral and cellular immunity for many years after supposed viral clearance and could present a potential risk for transmission or infection reactivation."

It would then be dependent on how long active virus can remain hidden. Does SVR ever mean complete absence of HCV RNA? If we're to believe the research, then no, it doesn't. I do think that the longer an individual maintains SVR, the likelihood of relapse (reactivation) remains low (<.5%). At least that's the anecdotal evidence I keep reading about. We haven't witnessed the number of successes we are now. So I think in the decade or two to come, we'll have the opportunity to collect the data that will provide the answer. By then, treatment will have improved so much, this will probably be a mute point. I don't think we're far off now.

In the meantime, like Pablo, I'm not going to worry about it



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Tig

67yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 9+ years!

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Greetings,

I do greatly enjoy such banter so as to keep the Grey Matter exercised.

With that then, I would like to see some thoughts on this scenario.

A person named Jed comes into contact with HCV in 1960. He does not know that. Years later, in the year 2000 he attempts to donate blood and is rejected because that have found the HCV AB.

He goes in for further tests, still early Y2K. He comes back UND and his Doctor explains that roughly 25% of people who come into contact with HCV fight it off with their own immune system.

Fast forward to the year 2020, Jed begins to show his age and it is noted that his immune system is compromised.

Can the 1960 contact now lead to a detectable HCV RNA?

Thinking caps required. wink

 

JimmyK

 



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Harvoni TX 2 12 weeks. UND weeks 4, 12 and now EOT + 4 Weeks. SVR-12 09/29/16. All Glory, Honor and Thanks be to God.

"I go to war with the brothers I trust."



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Interesting read indeed.

I must profess I find the whole topic confusing despite having read widely around the issues and having had it explained to me by doctors.

Why do a small percentage of people relapse after treatment when nearly everybody becomes UND at some point during DAA treatment?  

The most cogent theory is that small amounts of HCV persist below the cut-point and that UND is not no viral RNA present but, moreover, a small amount of RNA may still exist below the cut-off.   But then, confusingly, we get the scenario wherein a small percentage of people who are not UND at the end of treatment go on the achieve SVR.  The thinking being that the remaining RNA are mutations without the ability to replicate properly and die off over time.  But then we also know that that relapses are caused by resistance associated variations.  So it seems that some mutations can replicate and others not.

Then you have the issue that only 65% of people improve their fibrosis score after achieving SVR with the remaining 35% being split fairly evenly between no improvement and a worsening of fibrosis. Surely one would expect nearly everyone to improve after SVR?  Is it the case that, as per the linked paper below, that some viral RNA persists in some people's livers and therefore they don't improve despite their plasma being UND?

My brain begins to hurt when I think about these things!  I think the bottom line is that the science isn't fully understood around this yet.  So I am going to keep things simple:

-95% of people achieve SVR with DAAs;

-for the 5% of so who don't achieve SVR then a second, or even third, round of treatment with a different combo of DAAs for a longer period will work;

- the majority majority of people who achieve SVR will improve in terms of fibrosis;

- I'm going to take charge of the things that I can to keep my liver in good nick, e.g. not drinking alcohol;

- I will leave the speculation around what UND really means and whether the virus persists in a low grade form to the scientists, and not worry myself unduly about things I have no control over; for I know my own mind and I can work myself into a tizzy about such matters.

Amen.

Pablo



-- Edited by Pablito on Thursday 30th of June 2016 11:24:21 AM

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44 y.o. male, HCV G4 since 1996, F-scan score 9, F2, Failed prior I/R, finished sof/vel/vox 8 weeks 5/16, pre-treatment VL 2 million, EOT UND, EOT+4 UND, EOT+12 UND.

Tig


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My thought is all treatment drugs block the virus' ability to replicate. When the viral load is low enough or undetected and kept there long enough, to assure adequate tissue perfusion, the body's immune system takes over the job. If there are viable viral particles (capable of replication) anywhere, and the immune system experiences a failure or crisis, there is a possibility of relapse. Post mortem studies on people that had experienced a SVR, have found viral evidence capable of reproduction. The immune system function is key in maintaining SVR. 



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Tig

67yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 9+ years!

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Skewed,

Interesting (from 2005), but still .... good topic. Would have to search to see what else is "out there" on this topic (with the new daa's) and not just this one (from the old interferon days as you noted). Found persisting, 9 years! - interesting.

Mallani made mention of this (being in lymphocytes) and kind of on the side, another further conversation ensued about any possibility of fluctuating VL's coinciding/corresponding with with lymphocytes numbers. (See - "General Discussion - RE: Lymphocytes? (like Mallani said)!?".

smile C.



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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I wonder if the results are the same For all those who did sof along with the peg-RIBA 

also interesting that SVR blood has the potential to infect others with blood to blood contact?



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 M-64) 3 Treatments)( SOF-RIBA 2014)(SOF-RIBA-PEG 2016)(HCC 2016) (LIVER TRANSPLANT 8-2017)(VOSEVI-RIBA 2017)   SVR-12. 3-13-18   



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I ran across a white paper that answers this question with the older treatment (interferon and ribavirin). Here is the link to the paper: http://onlinelibrary.wiley.com/doi/10.1002/hep.20518/pdf

However, If anyone knows of a similar study done on SVR patients with the new DAA's, I would love to hear from you.

 

Cheers,

Skewed



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Diag. with hep c in 1992; A3:F2;  GT 1a; IL28B CT; VL 900k, ALT 150, AST 100 on 8/5/2014; SOT 9/5/2014  S/O ---VL 127 after 6 days; VL detected on day 18 but < 15.; --> UND @ EOT+ 1 year SVR!

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