Yes thanks for this Malcolm, you`re a mine of helpful information!
Incidentally we used to have a member who claimed that her genotype had changed and gave the explanation that her first course of tx (unsuccessful) had suppressed one type and so had allowed the second type to become dominant. I`ve no idea how true that was and it did cause some controversy at the time.
I came across this article a little while ago about a study of mixed genotypes in Pakistan, if anyone`s interested...
I do feel a book coming on- 'How to spend 48 weeks in a recliner-chair and bed while remaining fairly sane'!
Thank you all for your comments- it's therapeutic for me as I try to stop my brain from becoming as atrophied as my muscles.
mallani said
Nov 22, 2012
Dave, sorry, I didn't respond to your 'other forum' post. I've never seen anything in print with that scenario. Anything is possible, I guess. It sounds a bit unlikely.
Shep said
Nov 22, 2012
Malcolm--you continue to amaze me and help me to understand! I have always wondered what the difference betwee 1a and b's were. Hope you are doing well!
JoAnneh said
Nov 22, 2012
Malcomb,write a book for Hep C doctors too! Trish, it will be nice to get pass this disease. Bill,how have you endured over a year of Interferon, I hope you are doing okay w more energy than I. Lets keep working for a cure:) JoAnne
davesf said
Nov 22, 2012
On another forum someone posted that their genotype changed during treatment. Doctor's theory was that one was dominant in the test but during treatment that one dropped first so then the other one was dominant for the test.
Don't know if that's true but thought I'd pass the info along.
Bills said
Nov 22, 2012
I Think Malcom is on his way to writing a book
HCV for beginers to experts Thanks Malcom
mallani said
Nov 21, 2012
Hi Northern and Dave, the question of different Genotype infections is very interesting. Some posts on this forum mention patients whose Genotype had apparently changed over the years. Some of this may have been Lab error, as the old Genotype testing kits from the late 1990's and early 2000's were not as accurate. Infection by more than one Geno. does occur and seems to be geographical, being more likely in less developed countries ? why.
As each Genotype genome is different enough in structure, we can rule out mutation as a cause for change of Geno. If a patient has two Genotypes, this can only be acquired by two separate infections. This is why it is more likely in IV drug users who continue to share, or in patients who required multiple blood transfusions ( before blood was screened). eg if a bag of blood contained HCV Geno 1a, and another bag of blood contained Geno 3a, the patient may end up co-infected with Geno 1a and 3a. These were called 'super-infections' and there was a case report of a young female IV drug-user, who actually died of acute HepC hepatitis from a super-infection. Patients infected by two Geno's were thought to have a poor response to Rx.
Another report mentions a patient who had Geno 1a and 1b co-infection ( similar VL's). Some years later, without any Rx, only 1b was detectable. Reasons postulated were that the body's immune response could cope with one Geno., allowing the other to 'take-over'. It's obviously a complex issue, and must be a nightmare from a treatment point of view.
-- Edited by mallani on Thursday 22nd of November 2012 01:56:15 AM
LUV2RYDE said
Nov 21, 2012
Malcom,
Great post...alot of info to think over. If my trial ever begins....hoping by this month it does ....I hope I clear it so I can move on with my life.
Northern said
Nov 21, 2012
Have you ever heard about someone being infected with 2 different geno types?
davesf said
Nov 21, 2012
Another great post Malcolm. We really appreciate you taking a vast complex topic and breaking it down into bite size chunks with language that us laymen can understand.
Best, Dave
mallani said
Nov 21, 2012
Since the 1990's, volumes have been written about the differences between Genotype 1a and Genotype 1b. Researchers have gone to extraordinary lengths to try to highlight any differences. This is a summary of what was thought, and how it is today with the new Trial drugs.
The geographical distribution is well known- 1a is more common in the USA, and 1b is more common in Europe and Australasia. An initial huge survey found that 1a was more common in a younger age group- somehow this translated into 1a being more associated with IV drug users. The survey found 20-30% of 1b's had not obvious cause of infection, so it was more socially acceptable. Many subsequant studies failed to confirm this. Initial studies with interferon and ribavirin showed much better SVR rates with 1a . Other papers showed 1b was associated with a more aggressive disease progress, with cirrhosis being much more common in the 1b's. So, although not socially acceptable, 1a was the one to have. When I had my first course of Inter. and Riba. in 1998, I was fed this rubbish. Needless to say, over the years, all of the above has been disproved.
The only real difference between the two is the resistance to mutation. 1b is quite stable in structure, and requires at least 3 complex chemical reactions to form a mutation. Many believe this is the original 'in-the-wild' virus from which all other Genotypes and subgroups have evolved. 1a is quite unstable and only requires one ( some say two) simple chemical reactions to mutate. This is becoming more important with the DAA's, where RAVs are becoming so important. It was thought that this would be reflected in different SVR rates using the first generation protease inhibitors (Incivek and Victrelis). Theoretically, 1b's should do better. This has not translated into fact, although, with most of the results coming from the USA, there should be a higher % of 1a's.
With the new trials, some have found a distinct difference in SVR. One trial calls them the 'harder-to-treat 1a's', and has resulted in having to use Peg. for the 1a's (in additional to their new ****tail). In the same trial, the 1b's achieved 100% SVR12. It will be interesting to follow this when we get more Phase3 results, with greater numbers.
Not that it makes much difference- you can't chance your Genotype. I'd rather be a 2!
Yes thanks for this Malcolm, you`re a mine of helpful information!
Incidentally we used to have a member who claimed that her genotype had changed and gave the explanation that her first course of tx (unsuccessful) had suppressed one type and so had allowed the second type to become dominant. I`ve no idea how true that was and it did cause some controversy at the time.
I came across this article a little while ago about a study of mixed genotypes in Pakistan, if anyone`s interested...
http://wwwnc.cdc.gov/eid/article/17/8/10-0950_article.htm
I do feel a book coming on- 'How to spend 48 weeks in a recliner-chair and bed while remaining fairly sane'!
Thank you all for your comments- it's therapeutic for me as I try to stop my brain from becoming as atrophied as my muscles.
Dave, sorry, I didn't respond to your 'other forum' post. I've never seen anything in print with that scenario. Anything is possible, I guess. It sounds a bit unlikely.
Trish, it will be nice to get pass this disease.
Bill,how have you endured over a year of Interferon,
I hope you are doing okay w more energy than I.
Lets keep working for a cure:)
JoAnne
On another forum someone posted that their genotype changed during treatment. Doctor's theory was that one was dominant in the test but during treatment that one dropped first so then the other one was dominant for the test.
Don't know if that's true but thought I'd pass the info along.
I Think Malcom is on his way to writing a book
HCV for beginers to experts Thanks Malcom
Hi Northern and Dave, the question of different Genotype infections is very interesting. Some posts on this forum mention patients whose Genotype had apparently changed over the years. Some of this may have been Lab error, as the old Genotype testing kits from the late 1990's and early 2000's were not as accurate. Infection by more than one Geno. does occur and seems to be geographical, being more likely in less developed countries ? why.
As each Genotype genome is different enough in structure, we can rule out mutation as a cause for change of Geno. If a patient has two Genotypes, this can only be acquired by two separate infections. This is why it is more likely in IV drug users who continue to share, or in patients who required multiple blood transfusions ( before blood was screened). eg if a bag of blood contained HCV Geno 1a, and another bag of blood contained Geno 3a, the patient may end up co-infected with Geno 1a and 3a. These were called 'super-infections' and there was a case report of a young female IV drug-user, who actually died of acute HepC hepatitis from a super-infection. Patients infected by two Geno's were thought to have a poor response to Rx.
Another report mentions a patient who had Geno 1a and 1b co-infection ( similar VL's). Some years later, without any Rx, only 1b was detectable. Reasons postulated were that the body's immune response could cope with one Geno., allowing the other to 'take-over'. It's obviously a complex issue, and must be a nightmare from a treatment point of view.
-- Edited by mallani on Thursday 22nd of November 2012 01:56:15 AM
Malcom,
Great post...alot of info to think over. If my trial ever begins....hoping by this month it does ....I hope I clear it so I can move on with my life.
Since the 1990's, volumes have been written about the differences between Genotype 1a and Genotype 1b. Researchers have gone to extraordinary lengths to try to highlight any differences. This is a summary of what was thought, and how it is today with the new Trial drugs.
The geographical distribution is well known- 1a is more common in the USA, and 1b is more common in Europe and Australasia. An initial huge survey found that 1a was more common in a younger age group- somehow this translated into 1a being more associated with IV drug users. The survey found 20-30% of 1b's had not obvious cause of infection, so it was more socially acceptable. Many subsequant studies failed to confirm this. Initial studies with interferon and ribavirin showed much better SVR rates with 1a . Other papers showed 1b was associated with a more aggressive disease progress, with cirrhosis being much more common in the 1b's. So, although not socially acceptable, 1a was the one to have. When I had my first course of Inter. and Riba. in 1998, I was fed this rubbish. Needless to say, over the years, all of the above has been disproved.
The only real difference between the two is the resistance to mutation. 1b is quite stable in structure, and requires at least 3 complex chemical reactions to form a mutation. Many believe this is the original 'in-the-wild' virus from which all other Genotypes and subgroups have evolved. 1a is quite unstable and only requires one ( some say two) simple chemical reactions to mutate. This is becoming more important with the DAA's, where RAVs are becoming so important. It was thought that this would be reflected in different SVR rates using the first generation protease inhibitors (Incivek and Victrelis). Theoretically, 1b's should do better. This has not translated into fact, although, with most of the results coming from the USA, there should be a higher % of 1a's.
With the new trials, some have found a distinct difference in SVR. One trial calls them the 'harder-to-treat 1a's', and has resulted in having to use Peg. for the 1a's (in additional to their new ****tail). In the same trial, the 1b's achieved 100% SVR12. It will be interesting to follow this when we get more Phase3 results, with greater numbers.
Not that it makes much difference- you can't chance your Genotype. I'd rather be a 2!