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Author Topic: Risk of having a genetic mutation.  (Read 7008 times)

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Offline worried55

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  • Posts: 34
Risk of having a genetic mutation.
« on: May 06, 2016, 09:16:50 am »
I'm ending week 4 treatment on Sovaldi and dacklinza for type 3a.  Just had bloodwork done and waiting for results.   Very nervous!   I'm wondering what are the odds of having a genetic mutation and not getting an svr12?  I'm staying positive but it's still in the back of my mind!  I'm blessed to even get my meds and I am very hopeful!
3a
Diagnosed summer 2014
Infected somewhere between 2009 and 2014. 
Source unknown possibly tattoos or dentist
Started treatment April 2016 Sovaldi and dacklinza
Viral load to start 28,000
4 wk labs... Undetected!!!!!!!
8 wk labs.....Undetected!!!!!
12 wk labs.....(really 14 weeks. Taken 2 weeks post treatment)  Undetected!!!!!
24 wk labs.   Undetected!  Cured!

Offline Lynn K

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  • Member
  • Posts: 4,543
  • Get tested, get treated, get cured, fight Hep c!
Re: Risk of having a genetic mutation.
« Reply #1 on: May 06, 2016, 09:44:09 am »
Depending on your individual situation as I do not know your prior treatment history I would guess about 2 percent

I did see Sovaldi and daklinza is approved for GT 3 and for those who were never treated before without cirrhosis in the ALLY study SVR rates were 98% so I would say the odds are on your side

I assume you are speaking of the Y93H polymorphism I did find this study from the National Institute of Health

http://www.ncbi.nlm.nih.gov/pubmed/23384816

Natural prevalence of NS5A polymorphisms in subjects infected with hepatitis C virus genotype 3 and their effects on the antiviral activity of NS5A inhibitors.

RESULTS:
Phylogenetic analysis revealed a broad distribution with no significant geographic clustering. GT1 DCV resistance-associated variants (RAVs) were observed in GT3 subjects; variants (and their frequencies) included 28M/V (1%), 30A/K/S/T/V (10%), 31L/M (1%), E92A (1%) and Y93H (8.3%).

So what I get from that is the odds of you having the polymorphism that has the greatest effect on Sovaldi daklinza treatment, the Y93H, the prevalence seems to be about 8.3% that you would have that particular polymorphism
Genotype 1a
1978 contracted, 1990 Dx
1995 Intron A failed
2001 Interferon Riba null response
2003 Pegintron Riba trial med null response
2008 F4 Cirrhosis Bx
2014 12 week Sov/Oly relapse
10/14 fibroscan 27 PLT 96
2014 24 weeks Harvoni 15 weeks Riba
5/4/15 EOT not detected, ALT 21, AST 20
4 week post not detected, ALT 26, AST 28
12 week post NOT DETECTED (07/27/15)
ALT 29, AST 27 PLT 92
24 week post NOT DETECTED! (10/19/15)
44 weeks (3/11/16)  fibroscan 33, PLT 111, HCV NOT DETECTED!
I AM FREE!

Offline worried55

  • Member
  • Posts: 34
Re: Risk of having a genetic mutation.
« Reply #2 on: May 06, 2016, 09:54:56 am »
Thank you for the reply! I've had this somewhere in the last 5 years.  I'm only f0-1.  I have absolutely no symptoms except fatigue but that is gone since starting the meds!  My last viral load was only 32,000 so with that low number of copies I'm hoping that there is even less of a chance that any of them have morphed!  The statistics are definitely in my favor!
3a
Diagnosed summer 2014
Infected somewhere between 2009 and 2014. 
Source unknown possibly tattoos or dentist
Started treatment April 2016 Sovaldi and dacklinza
Viral load to start 28,000
4 wk labs... Undetected!!!!!!!
8 wk labs.....Undetected!!!!!
12 wk labs.....(really 14 weeks. Taken 2 weeks post treatment)  Undetected!!!!!
24 wk labs.   Undetected!  Cured!

Offline Lynn K

  • Global Moderator
  • Member
  • Posts: 4,543
  • Get tested, get treated, get cured, fight Hep c!
Re: Risk of having a genetic mutation.
« Reply #3 on: May 06, 2016, 10:08:53 am »
Most people with hep c do not have symptoms which is why hep c is called a silent illness people generally do not have symptoms unless the develop cirrhosis and the symptoms then are those of cirrhosis. Otherwise the most frequently reported symptom is tiredness.

Others do have more difficulty with hep c and even can develop extra hepatic symptoms.

The general lack of symptoms is why those born between 1945 to 1965 (baby boomers) are urged by the CDC to be tested for hep c as that age group seems to be most at risk for undiagnosed hep c
Genotype 1a
1978 contracted, 1990 Dx
1995 Intron A failed
2001 Interferon Riba null response
2003 Pegintron Riba trial med null response
2008 F4 Cirrhosis Bx
2014 12 week Sov/Oly relapse
10/14 fibroscan 27 PLT 96
2014 24 weeks Harvoni 15 weeks Riba
5/4/15 EOT not detected, ALT 21, AST 20
4 week post not detected, ALT 26, AST 28
12 week post NOT DETECTED (07/27/15)
ALT 29, AST 27 PLT 92
24 week post NOT DETECTED! (10/19/15)
44 weeks (3/11/16)  fibroscan 33, PLT 111, HCV NOT DETECTED!
I AM FREE!

Offline Luna7

  • Member
  • Posts: 179
Re: Risk of having a genetic mutation.
« Reply #4 on: May 06, 2016, 12:11:23 pm »
I'm 2 weeks behind you, Worried, same genotype, same meds. Will take my 15th dose today.
The odds are in our favor!
Between F2 & F3
Alt & Ast nearly 100
Viral load over 8 million
Gt 3a

Treated 12 weeks with Sovaldi & Daklinza, start date mid-April 2016
Undetected at 4 weeks into treatment
Alt & Ast  normal
Treatment completed July 14
Most likely will be undetected at 12 weeks (mid October 2016) as symptoms are gone

Offline FutureThinker

  • Member
  • Posts: 711
  • Onward and upward!
Re: Risk of having a genetic mutation.
« Reply #5 on: May 06, 2016, 01:10:25 pm »
Worried and others, I have given this issue of RAVs a great deal of thought over the past 12 months, while I was fighting to get coverage for my treatment.  I was actually considering finding some way to pay for the Harvoni out of pocket if necessary -- so the issue of RAVs was very important in view of that kind of cost.
The FDA trials (clinicaltrials.gov) that are online for all DAAs provide fairly easy-to-read data for all aspects of these treatments, so check those out for more detailed info.

Merck's Zepatier guidelines are the only DAA thus far to require PRE-TREATMENT RAV testing. I do believe there will be a much more "personalized" pre-treatment workup in the near future before prescribing any of these DAAs.  We are just not there yet, as we are still learning a lot about this disease.

Also, just as important -- the RAVs can also develop DURING TREATMENT.  So, between the very low possibility of having a mutation prior to treatment, or then developing resistance during treatment, right now, you just won't know until you go thru treatment.

So -- my recommendation is don't waste a lot of energy on if you have the polymorphisms or not. It's not productive....think positive thoughts!! You either have them or you don't, or you might develop them or not -- it has nothing to do with VL or F score -- it's your DNA. And it's a very low percentage. Also, trials are going on right now to treat relapsers, and new drugs are coming out this year and next, so there is a great deal of hope now that if one drug doesn't work, another will, and in the near future. That's not the scenario we want, but at least there are now some good options. We are blessed to be getting treatment at this time, as compared to so many others in the not-so-distant past.

As Lynn K has written in the past and I read often, "Don't borrow worry and disappointment from a tomorrow that may never come." Excellent advice for those of us on treatment. Stay positive and focus on getting to the other side , FT
Treatment naive
Likely contracted mid-70s
Diagnosed 1a, 2011
F1-2
Harvoni X 12 weeks, completed 5/17/16
Pre-treatment: VL 3 mil, AST 64, ALT 84
4 week labs: VL 30, AST 21, ALT 14
8 week labs: VL UD!!!, AST 22, ALT 16
12 week labs: VL UD, AST 23, ALT 14
2 wk EOT: VL UD
12 wk EOT: VL UD, AST 22, ALT 13 =  SVR 12! Yay! 
Last hep appointment: VL UD, AST 19, ALT 12 = SVR 39! I AM DONE!

 


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