Hi Paul, thanks for posting the link, I`ve read about that before. Yes you`re right, I was just describing a theory which really applies more to the older SOC Peg/rib based treatments, and I`m sure that as we get more post treatment data from the new DAA drugs we`ll see more cases like yours, which is very encouraging.
Thanks Tess, that`s a good point, we all should follow good hygiene practice anyway whenever blood contact is a possibility.
Tess said
Jun 13, 2015
boostm, thank you for posting this. It makes sense --
"there are many examples with harvoni where low detecteds at EOT resolve to SVR12. The idea is that the low quantification amounts at eot represent impotent disabled virions which cannot replicate and therefore, are not contagious and, for all intents and purposes, are dead."
KPB - As far as I can tell no one really knows for certain if there is a chance of passing on the virus after SVR. But what we have learned over the past few decades is that everyone must be vigilant about blood contamination whether they've ever been diagnosed with a blood borne virus or not. Those of us with HCV or HIV, etc. are especially aware, but everyone needs to be careful not to share razors, toothbrushes, etc., and to be careful not to expose themselves to others' blood. So other than not being able to donate blood, if someone reaches SVR they're basically the same as everyone else regarding blood.
- Tess
boostm3 said
Jun 13, 2015
CG, Ive read different interpretations of what it means to be SVR with Harvoni... The theory you quoted is that SVR means the value of your viral load is below that which can be quantified by the test, or below the LOD for that test.. and because the numbers are tiny, the immune system keeps them in check. However, other 'theories' say that HCV that cant replicate is impotent and non vital.. Unlike interferon, Harvoni stops the virus from replicating, so that once you achieve UND status, the virus is for all intents and purposes dysfunctional and not vital... If it cant replicate, it dies off.
At my 8wk end of treatment, my vl was 29. At 7.5 wks post treatment, it had dropped to detected < 15. And at 11 wks post treatment, I hit the svr jackpot being UND for the first time. With interferon, this progression couldnt have happened... a detected vl at EOT no matter how small would generally replicate rapidly after that. But there are many examples with harvoni where low detecteds at EOT resolve to SVR12. The idea is that the low quantification amounts at eot represent impotent disabled virions which cannot replicate and therefore, are not contagious and, for all intents and purposes, are dead.
As for donating blood, I read that once a screen returns positive for the HCV antibodies, rather than incur the expense of the more expensive viral load tests, they simply deny you as a donor.
-- Edited by boostm3 on Sunday 14th of June 2015 03:38:45 AM
-- Edited by boostm3 on Sunday 14th of June 2015 03:53:40 AM
-- Edited by boostm3 on Sunday 14th of June 2015 04:09:30 AM
Cinnamon Girl said
Jun 13, 2015
Yes, that is a way of understanding why when our treatment is successful it`s referred to as achieving `SVR` rather than a `cure`.
And following on from that, yes there would, theoretically at least, be a minimal possibility of infecting someone else, which is why we are not allowed to donate blood ever again once we`ve had Hep C, even after SVR.
But this isn`t something we need to worry unduly about, it`s mostly just theoretical. I achieved SVR and like most people who do, I consider myself to be`cured`. It`s just something to be aware of.
KPB said
Jun 13, 2015
Thank you for answering Cinnamon Girl,
So... what I think you are saying is::: we are not cured... but our virus has been reduced to a level that it will not damage our bodies any further.
Now, If the above statement is true....?
And if we are still carriers of this hep c infection, then I would think other people are still in danger of contracting this infection from us.
would that also be a true statement ????
Cinnamon Girl said
Jun 13, 2015
Hi KPB, that`s a good question and I`ll try to explain briefly.
When we reach SVR it means that there has been no detectable quantity of the virus in our bloodstream for at least 12 weeks after the end of treatment, which is the nearest we have to a `cure` because the chances of relapse after that point are so low. At that stage it means that we no longer have an active infection. But because it`s impossible to measure below the lowest quantifiable levels of the existing PCR viral load tests then theroretically there still could be a very tiny amount of virus in our bodies which in usual circumstance our own immune systems can keep under control and prevent from multiplying.
In medical terms though it isn`t usually referred to as a cure because we haven`t reached the stage of getting 100 % success rates for any drug yet.
Hope that helps to explain the situation.
KPB said
Jun 13, 2015
Two weeks ago, I asked the question below. You can also see the answers I received to my question. But since I am considered the ("ignorant"general public that may understand the whole SVR/cure debate ) I was wondering if anyone could explain it to me in layman terms ?
I still do not understand
KPB wrote: (two weeks ago)
I am confused about relapse, if Harvoni claims to cure Hep C, then how is it possible to relapse ?
Harvoni doesn't claim to cure HepC. It claims it can reduce the amount of virus in the peripheral blood to an Undetected amount, usually <15 i.u./ml, 12-24 weeks after finishing treatment.
Actually, a TV commercial for Harvoni in the U.S. claims a "96 to 99% cure rate" not SVR. I was confused about this at first, but realized the it is aimed at the "ignorant"general public that may understand the whole SVR/cure debate.
Hi Paul, thanks for posting the link, I`ve read about that before. Yes you`re right, I was just describing a theory which really applies more to the older SOC Peg/rib based treatments, and I`m sure that as we get more post treatment data from the new DAA drugs we`ll see more cases like yours, which is very encouraging.
Thanks Tess, that`s a good point, we all should follow good hygiene practice anyway whenever blood contact is a possibility.
boostm, thank you for posting this. It makes sense --
"there are many examples with harvoni where low detecteds at EOT resolve to SVR12. The idea is that the low quantification amounts at eot represent impotent disabled virions which cannot replicate and therefore, are not contagious and, for all intents and purposes, are dead."
KPB - As far as I can tell no one really knows for certain if there is a chance of passing on the virus after SVR. But what we have learned over the past few decades is that everyone must be vigilant about blood contamination whether they've ever been diagnosed with a blood borne virus or not. Those of us with HCV or HIV, etc. are especially aware, but everyone needs to be careful not to share razors, toothbrushes, etc., and to be careful not to expose themselves to others' blood. So other than not being able to donate blood, if someone reaches SVR they're basically the same as everyone else regarding blood.
- Tess
CG, Ive read different interpretations of what it means to be SVR with Harvoni... The theory you quoted is that SVR means the value of your viral load is below that which can be quantified by the test, or below the LOD for that test.. and because the numbers are tiny, the immune system keeps them in check. However, other 'theories' say that HCV that cant replicate is impotent and non vital.. Unlike interferon, Harvoni stops the virus from replicating, so that once you achieve UND status, the virus is for all intents and purposes dysfunctional and not vital... If it cant replicate, it dies off.
At my 8wk end of treatment, my vl was 29. At 7.5 wks post treatment, it had dropped to detected < 15. And at 11 wks post treatment, I hit the svr jackpot being UND for the first time. With interferon, this progression couldnt have happened... a detected vl at EOT no matter how small would generally replicate rapidly after that. But there are many examples with harvoni where low detecteds at EOT resolve to SVR12. The idea is that the low quantification amounts at eot represent impotent disabled virions which cannot replicate and therefore, are not contagious and, for all intents and purposes, are dead.
http://cid.oxfordjournals.org/content/early/2015/03/02/cid.civ170.abstract
As for donating blood, I read that once a screen returns positive for the HCV antibodies, rather than incur the expense of the more expensive viral load tests, they simply deny you as a donor.
-- Edited by boostm3 on Sunday 14th of June 2015 03:38:45 AM
-- Edited by boostm3 on Sunday 14th of June 2015 03:53:40 AM
-- Edited by boostm3 on Sunday 14th of June 2015 04:09:30 AM
Yes, that is a way of understanding why when our treatment is successful it`s referred to as achieving `SVR` rather than a `cure`.
And following on from that, yes there would, theoretically at least, be a minimal possibility of infecting someone else, which is why we are not allowed to donate blood ever again once we`ve had Hep C, even after SVR.
But this isn`t something we need to worry unduly about, it`s mostly just theoretical. I achieved SVR and like most people who do, I consider myself to be`cured`. It`s just something to be aware of.
Thank you for answering Cinnamon Girl,
So... what I think you are saying is::: we are not cured... but our virus has been reduced to a level that it will not damage our bodies any further.
Now, If the above statement is true....?
And if we are still carriers of this hep c infection, then I would think other people are still in danger of contracting this infection from us.
would that also be a true statement ????
Hi KPB, that`s a good question and I`ll try to explain briefly.
When we reach SVR it means that there has been no detectable quantity of the virus in our bloodstream for at least 12 weeks after the end of treatment, which is the nearest we have to a `cure` because the chances of relapse after that point are so low. At that stage it means that we no longer have an active infection. But because it`s impossible to measure below the lowest quantifiable levels of the existing PCR viral load tests then theroretically there still could be a very tiny amount of virus in our bodies which in usual circumstance our own immune systems can keep under control and prevent from multiplying.
In medical terms though it isn`t usually referred to as a cure because we haven`t reached the stage of getting 100 % success rates for any drug yet.
Hope that helps to explain the situation.
Two weeks ago, I asked the question below. You can also see the answers I received to my question. But since I am considered the ("ignorant"general public that may understand the whole SVR/cure debate ) I was wondering if anyone could explain it to me in layman terms ?
I still do not understand
Harvoni doesn't claim to cure HepC. It claims it can reduce the amount of virus in the peripheral blood to an Undetected amount, usually <15 i.u./ml, 12-24 weeks after finishing treatment.
Actually, a TV commercial for Harvoni in the U.S. claims a "96 to 99% cure rate" not SVR. I was confused about this at first, but realized the it is aimed at the "ignorant"general public that may understand the whole SVR/cure debate.
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