How long a single virus can live in my system without replicating?

[zufa12k]

Does anyone know how long a single virus can live in my system without replicating?
I am taking a protease and polymerase along with the standard SOC.
I know the DAA attack the virus when it is trying to replicate. If the virus isn’t replicating the DAA don’t touch it.

I am a non responder 2x, this is my 3rd try. The Pegasus and Copegasus weren’t very effective in attacking the virus (I am genotype 1a IL28B CT) when I isn’t replicating.  For me to stay UND I need to virus to try to replicate so the DAA will kill it (or so I believe)

[tttppp]

There was a ride at Six Flags Over Georgia 36 years ago, it was a round room, 30 feet in diameter. People stood against the wall and the room spun around and then the floor dropped down. The people stayed against the wall and didn't drop. I think the virus was pushed against the host cells back wall and couldn't eat good or split. The DNA strands, which have to be extremly complecated, couldn't split because they were stuck against the back wall and couldn't move at all. Even the ones in the blood stream couldn't split good enough. So, if the viruse life span is short, all the viruse would die before a lot of cells.

[nomorehepcliz]

are you on the BMS trial, with 790052 or 650032 or the placebo? there is an interesting article somewhere, I will try to find it about how the IL28B genotypes respond to Telaprevir - the TT does the best but CT does well also.  I am CC.  I wonder if your CT allele explains why you are a non responder.

Hector, very interesting, thanks!

[screaming48]

Thank you! That does make me feel better, I just don't understand all this all the time, I appreciate you answering..all the best to you as well.

[zufa12k]

Hectorsf - thank you for your informative post, nice to get good information.

I didn't state it correctly re wanting the virus to replicate. I was trying to communicate my fear re my two DAA only working on the virus when it is replicating and even if one virus was lurking around in a monk like state (not replicating) it would replicate when I stop my DAA in 5 months.
As you stated a single virus must replicate or die, a single virus has a short, but potentially prolific 'natural' lifespan.

Your explanation of the role of Peg-interferon and ribavirin on mutants makes sense to me. As a 2x non-responder I was wondering what the value of Peg-interferon and ribavirin was for me.

As I have gone from 12,000,000 to UND in 2 weeks, still UND at 4 weeks I am now more confident.

Screaming48 – my clinic trial is different than yours, but the new direct acting antivirals are having some amazing results. The viral load can really bounce around. My screening was 9,000,000, 1 week later my base line was 12,000,000. If you have 13.9 mil I wouldn’t be overly concerned, when teleprevir starts the killing I don't think a few mil either way won’t make a difference. All the best.
  

[screaming48]

I understand that viral load really has no bearing on the shape your liver is in. But I know it does have something to do with how it is treated, meaning I will treat for 48 weeks with teleprevir and soc. My question is will the treatment work that quickly with a viral load of 13.9 million? To me it feels like a disadvantage to have that high a viral load and try to be und or rvr at 4 weeks.(still learning the codes) Your thoughts on this would help Hector and anyone else who would like to chime in.. anne

[researchmonkey326]

Thank you for such an informative post.  

[HectorSF]

The virus is always replicating. If it wasn't replicating you wouldn't have chronic hepatitis C. If the virus doesn't replicate it dies. There are Billions and Billions (as Carl Sagan used to say) of hepatitis C viruses replicating every day normally. The DAA prevents replication. The peg-interferon and ribavirin kill off the remaining mutant viruses and keep the viruses from coming back.

So the premise that you want the viruses to replicate is mistaken.
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Definitions:
“Wild type” is the dominate virus
“Mutants” mutations of the parent “wild type” virus

* (First and foremost) Mutants are there all the time in every person with chronic HCV. HCV mutates more rapidly then HIV. HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, HCV also has an exceptionally high mutation rate, a factor that may help it elude the host's immune response.
* Mutants were first uncovered by Vertex using their “Population sequencing” model – hundred of PCR tests per time point yielding the entire sample of virus population.
* Vertex showed that the use of Telaprevir knocks down the main HCV virus “wild virus” 3-5 logs, this allowed the viewing of the mutants. The mutations are the majority of the virus that remain if a patient viral load plateaus or rebounds. I.E. Treatment does not eliminate the virus.
* RVR is a predictor of SRV because if the main or “wild virus” is driving down to zero quickly (within 4 weeks), no “parents” (wild viruses) exits to create the mutants.
* Peg-interferon and ribavirin role in the cocktail is to eliminate the remaining mutants.

If the main virus or “wild virus” is driving down to zero quickly (within 4 weeks for RVR), no “parents” (wild viruses) exits to create more mutants. Therefore both the main virus ("wide virus") plus all other mutations (acted on by Peg-interferon and ribavirin) are reduced to 0. This is one of the properties of the new antivirals that make them so effective. Quick drop of viral load of the main virus.

All this assumes the antiviral can reduce the main virus to UND. If not then the remaining mutants stay active and the patient viral load will either plateau or rebound over time. Since the main virus is the most "fit" of the viral variations, it again becomes the dominate virus. Remember that mutant virus exist in all patients, all the time. It is only when the main virus is suppressed that the mutants become the majority of the active viruses.
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Good luck with your treatment.

Hector

[his3707]

great question    lately I have wondered what the incevik is doing after Im undetectable.  I still really dont understand how the virus can hide as in undetectable while you are treating and then resurface after treatment stops.  I have not had the chance to ask the study nurse.  I hope someone with the knowledge will jump in here and give us an answer.  I am also lA and CT.  1st time around in the treatment arena and SURLEY better be my last!!