Aa
can you stop treatment oce you start
I'm hearing a lot of diffrent things about mutant virus's and that once you start treatment you will make your situation worse if you stop at some point. is this true?
Thanks
This discussion is related to Post Tx Side Effects.
Thanks
This discussion is related to Post Tx Side Effects.
Thanks for the Links.
Spectda- very informative and in laymen’s terms which makes it easy to follow and understand.
willing-I was only able to scan over yours but, I am looking foward to reading it when I get home.
Spectda- very informative and in laymen’s terms which makes it easy to follow and understand.
willing-I was only able to scan over yours but, I am looking foward to reading it when I get home.
added a little show-n-tell note for a specific mutation which may make the topic a bit more concrete:
http://www.medhelp.org/user_journals/show/198549
http://www.medhelp.org/user_journals/show/198549
this is a good article about mutations that occur even without therapy. The mutations always occur to trick your body into not attacking them.
http://www.hcvadvocate.org/hepatitis/Basics/New%20Antivirals_09.pdf
http://www.hcvadvocate.org/hepatitis/Basics/New%20Antivirals_09.pdf
Thanks for the responses (please bare with me, I am having a “fog moment”),
HectorSF- “First and foremost) Mutants are there all the time in every person with chronic HCV”
“ HCV also has an exceptionally high mutation rate, a factor that may help it elude the host's immune response.”
Spectda- “The mutations are important if they don't die off and they become dominant, then you are stuck with a resistant virus. That does not seem to be an issue with the current standard of care (interferon and ribavirin), just with new protease inhibitors like telaprevir and boceprevir”
HectorSF, your saying that HCV mutates on it’s own to elude the host’s immune response.
Spectda your saying HCV also mutates because of the new protease inhibitors.
I always thought HCV naturally mutates but I also thought SOC caused mutation, apparently I was wrong.
To sum it up (contrary to popular belief, I am not mentally challenged) Mutation is caused only by HCV’s natural defense and the new protease inhibitors. SOC plays no role in mutation
HectorSF- “First and foremost) Mutants are there all the time in every person with chronic HCV”
“ HCV also has an exceptionally high mutation rate, a factor that may help it elude the host's immune response.”
Spectda- “The mutations are important if they don't die off and they become dominant, then you are stuck with a resistant virus. That does not seem to be an issue with the current standard of care (interferon and ribavirin), just with new protease inhibitors like telaprevir and boceprevir”
HectorSF, your saying that HCV mutates on it’s own to elude the host’s immune response.
Spectda your saying HCV also mutates because of the new protease inhibitors.
I always thought HCV naturally mutates but I also thought SOC caused mutation, apparently I was wrong.
To sum it up (contrary to popular belief, I am not mentally challenged) Mutation is caused only by HCV’s natural defense and the new protease inhibitors. SOC plays no role in mutation
"I’m confused, I always thought HCV does mutate and this is what made it so hard to kill".
You are correct.
Main points about HCV viral mutants and variations:
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 – hundreds of PCR tests per time point yielding the entire sample of virus population.
* Because Telaprevir knocks down the main HCV virus “wild virus” 3-5 logs, this allowed for the first time 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.)
* When the main or “wild virus” is driven down to zero quickly, as is the case with STAT-C treatment no “parents” (wild viruses) exit to create the mutants.
* Peg-interferon and ribavirin are used to eliminate the remaining mutants. Thus elimanate the virus.
Hectorsf
You are correct.
Main points about HCV viral mutants and variations:
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 – hundreds of PCR tests per time point yielding the entire sample of virus population.
* Because Telaprevir knocks down the main HCV virus “wild virus” 3-5 logs, this allowed for the first time 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.)
* When the main or “wild virus” is driven down to zero quickly, as is the case with STAT-C treatment no “parents” (wild viruses) exit to create the mutants.
* Peg-interferon and ribavirin are used to eliminate the remaining mutants. Thus elimanate the virus.
Hectorsf
I am not sure about the odds of a second treatment when the first treatment is aborted. It seems like your odds on the second time would certainly not improve unless some other variable were changed such as insulin resistance, obesity, dosage, etc. Because of that, I question why you would want to quit once you have started. This seems like a bad idea. Why not finish TX and give yourself the best chances possible?
Polonius' advice to Laertes about entering a quarrel might be put to good use here.
Polonius' advice to Laertes about entering a quarrel might be put to good use here.
The mutations are important if they don't die off and they become dominant, then you are stuck with a resistant virus. That does not seem to be an issue with the current standard of care (interferon and ribavirin), just with new protease inhibitors like telaprevir and boceprevir. Often People treat with the current soc several times before they are cured.
I’m confused, I always thought HCV does mutate and this is what made it so hard to kill.
Even though I am from the "Watch and Wait Klan" (unless advanced liver damage), I believe once you made the commitment to start tx you should do everything in your power to complete it (if possible).
Even though I am from the "Watch and Wait Klan" (unless advanced liver damage), I believe once you made the commitment to start tx you should do everything in your power to complete it (if possible).
We have lots of members who have done treatment, relapsed, then retreated again (for a longer duration or with more meds or a different interferon) who have achieved SVR. If there truly were mutation issues with just standard of care meds then this could not happen.
Still in the 'olden' days we did always say that your first attempt at treatment is usually your best chance. There must have been a reason which I no longer remember or maybe this was disproven. I'd not quit treatment unless it was absolutely and totally necessary.
Still in the 'olden' days we did always say that your first attempt at treatment is usually your best chance. There must have been a reason which I no longer remember or maybe this was disproven. I'd not quit treatment unless it was absolutely and totally necessary.
If you don't have somewhat advanced damage to your liver then waiting for a combination of drugs that probably won't cause mutations, or going with the current soc (riba and interferon) is probably the best idea. If you have damage to your liver that is serious or close to it, then you have to weigh the risk of having your liver get worse against having the meds cause a mutation.
The information that I have read about boceprivir and telaprevir seem to suggest that most mutations die off eventually in people that were not successful with the treatment. Very occasionally the mutation becomes the dominant lasting strain.
The information that I have read about boceprivir and telaprevir seem to suggest that most mutations die off eventually in people that were not successful with the treatment. Very occasionally the mutation becomes the dominant lasting strain.
As inidcated, there does not appear to be any reports on the virus developing a resistance to the current TX meds.
As also indicated, this does not appear to be true of the new NOS agents (i.e. Polymerase and Protease) though which is why they are only being added during the initial phases of TX in order to allow the main engine TX meds (i.e. Inteferon and Ribaviron) to gain the upper hand.
I don't know that there has been any research to determine if the resistance to the NOS agents is a permanent mutation and as as such rendering them useless for future TX attempts if used during an attempt which fails to clear.
Some of the studies conducted on the NOS agents has been focused on determining if resisitance to the main TX meds has occurred and from what I've read or heard has not seen to be the case. The main concern there was causing a mutation which would produce strains of HCV which were resistant to exist TX meds.
From what I know, it seems that it is not clearly understood how Riba even works completely in halting replication so Interferon can kill the virus present. If it were would seem to be useful in finding a more potent means of completely halting replication entirely while Inteferon did it's thing.
How it currently seems to go is that the virus enters the body and begins mutating to reach a point where the persons immune system stops recognizing it as a threat and so quits attacking it. By introducing Interferon, you are in effect overriding the bodies recognition trigger to naturally produce IFN to attack the virus.
As far as retreating goes, there are success testimonies of folks have have undergone TX several times before attaining SVR. The most I have heard about to date is 5 times for one person I know.
However to retreat or not appears to be dependent upon the doctors view on possible chance of seeing SVR success which seems to vary. How a person reacts to TX also appears to be part of the equation on whether to retreat or not.
I believe what you may be hearing in discussions on not stopping is that since you are in a battle with the virus and may possibly have the upper hand on attaining SVR, why stop and let it regroup again? Unless of course you are experiencing extreme SX's which are focing you to stop.
As also indicated, this does not appear to be true of the new NOS agents (i.e. Polymerase and Protease) though which is why they are only being added during the initial phases of TX in order to allow the main engine TX meds (i.e. Inteferon and Ribaviron) to gain the upper hand.
I don't know that there has been any research to determine if the resistance to the NOS agents is a permanent mutation and as as such rendering them useless for future TX attempts if used during an attempt which fails to clear.
Some of the studies conducted on the NOS agents has been focused on determining if resisitance to the main TX meds has occurred and from what I've read or heard has not seen to be the case. The main concern there was causing a mutation which would produce strains of HCV which were resistant to exist TX meds.
From what I know, it seems that it is not clearly understood how Riba even works completely in halting replication so Interferon can kill the virus present. If it were would seem to be useful in finding a more potent means of completely halting replication entirely while Inteferon did it's thing.
How it currently seems to go is that the virus enters the body and begins mutating to reach a point where the persons immune system stops recognizing it as a threat and so quits attacking it. By introducing Interferon, you are in effect overriding the bodies recognition trigger to naturally produce IFN to attack the virus.
As far as retreating goes, there are success testimonies of folks have have undergone TX several times before attaining SVR. The most I have heard about to date is 5 times for one person I know.
However to retreat or not appears to be dependent upon the doctors view on possible chance of seeing SVR success which seems to vary. How a person reacts to TX also appears to be part of the equation on whether to retreat or not.
I believe what you may be hearing in discussions on not stopping is that since you are in a battle with the virus and may possibly have the upper hand on attaining SVR, why stop and let it regroup again? Unless of course you are experiencing extreme SX's which are focing you to stop.
when you say attaining a sustained virological responce, I'm assuming you mean during the present treatment plan. in other words if one was to stop for some reason, then start over again would they have the same chance of sustainment?
thank you for you help.
thank you for you help.
With the current standard of care people don't develop a resistance to the medications if they stop prior to the end of their scheduled treatment duration but it does decrease the odds of attaining a sustained virological response.
It has been shown that If SVR is not reached with the newer drugs (Protease and Polymerase Inhibitors) resistance does occur.
Trinity
It has been shown that If SVR is not reached with the newer drugs (Protease and Polymerase Inhibitors) resistance does occur.
Trinity
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