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Hep C Discussion Forum -> On Treatment -> About genotype three a
Post Info TOPIC: About genotype three a
Huey


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About genotype three a
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So if this is the case, my story starts when i was only 12. That is when i got it.  and now at 52 it has been detected and treatment started.   If you look at the study from the German woman that where infected by accident it says clinical shins appear after 35 years.  my:" time-line exactly".  along with the knowledge of my mothers various symptoms I came to the realization that I feel bad in all the places and ways mom did.  Before I was tested for Hep I complained about having some kind of genetic disease because I have the same symptoms as my mom.  Then when i ask about Hep the Dr said I didn't look yellow.  ?  .,  Finely  they tested.  It was later when i talked with my older Sister whom is a nurse ;now retired; that i found out our Mother had Hep non a non b.  She got it from a Blood transfusion at BenTob Hospital  in Houston Texas , this was around 1976. 



-- Edited by Huey on Saturday 10th of May 2014 08:39:55 PM

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  HCV Genotype 3a , now Psot-Tx was on S/riba. First VL was 5.8 mil on 7-5-13 then "und" at 3.8 weeks. 06/13/14 still und. off meds 3 days back on 7/29 Last pill 08/10/14 SVR+4

 
Cinnamon Girl


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Hi again, and welcome to the forum, Huey.

Thanks for the information, and yes you`re right it saying your mother would have had the same genotype as you if you caught it from her.  People with genotype 3 are more prone to having a `fatty liver` and that can cause problems sometimes.

Genotype 3 used to be considered one of the easiest to treat as people with that genotype usually respond very well to the older `standard of care` treatment combo of peginterferon and ribavirin (which is what I did), but it`s a different scenario with the newer PI treatments and with the new DAA drugs.  There are more new drug combos in the pipeline though which look as though they will be very effective across all genotypes so things are moving forward very quickly.

One thing I`d like to point out from the information you`ve quoted.  Where it says "HCV genotype 3 is more prevalent.....among intra-venous drug users"... while that used to be thought to be true it is in fact now considered outdated as anyone can catch any genotype through any activity which involves `blood to blood` contact, including intra-venous drug use. 

As genotype 3a you`ll be doing 24 weeks, and you have an excellent chance of a successful outcome with that length of treatment, which is based on the results of the clinical trials.  Sounds like your treatment is going well so far from what you`ve written on your whiteboard.

Wishing you all the best of luck!

(By the way, it`s very helpful if you could write a few words in your `signature` line just to say what treatment you`re on, your genotype, and your progress so far, and then it will show up underneath all your posts.  To do that just select `Signature` in your user details profile box. That helps us respond to your posts without having to keep looking back.  Thanks! )

 

 



__________________

Jill 

(71 yo, lives in UK)

Was Gen 3a, 

24wks Peg Ifn/Riba, Sep 2010 - Mch 2011

UND @ Wk.4, UND @ EOT, 

SVR Nov 2011 --> Still UND @ EOT + 4 yrs.

 

 
Huey


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J. Ampuero1,2, M. Romero-Gómez1 and K. R. Reddy2,*Article first published online: 20 FEB 2014
DOI: 10.1111/apt.12646
Summary
Background
Over the past several years, hepatitis C therapy has been pegylated interferon and ribavirin based. Although protease
inhibitor-based therapy has enhanced response rates in genotype 1, the recent advances in therapy have demonstrated a
challenge in genotype 3, a highly prevalent infection globally.
Aim
To provide a comprehensive summary of the literature evaluating the unique characteristics and evolving therapies
in genotype 3.
Methods
A structured search in PubMed, the Cochrane Library and EMBASE was performed using defined key words, including only full
text papers and abstracts in English.
Results
HCV genotype 3 is more prevalent in Asia and among intra-venous drug users. Furthermore, it interferes with lipid and glucose
metabolism, and the natural history involves a more rapid progression of liver disease and a higher incidence of hepatocellular
carcinoma (HCC). New therapies with protease inhibitors have focused on genotype 1 largely and have demonstrated
enhanced responses, but have limited activity against genotype 3. Thus far, in clinical trials, NS5B and NS5A inhibitors have
performed more poorly in genotype 3, while a cyclophilin inhibitor, alisporivir, has shown promise.
Conclusions
As treatments for HCV have evolved, genotype 3 has become the most difficult to treat. Furthermore, genotype 3 has special
characteristics, such as insulin resistance and alterations in lipid metabolism, which may partly explain the lower treatment
responses. A great deal of emphasis on advancing therapy is needed in this population that appears to have a more rapid
progression of liver disease and a higher incidence of HCC.

 

  This is vary interesting to me because it suggests that my mother must have had genotype 3 as I do because we both have a special characteristic not found in other genotypes.



__________________

  HCV Genotype 3a , now Psot-Tx was on S/riba. First VL was 5.8 mil on 7-5-13 then "und" at 3.8 weeks. 06/13/14 still und. off meds 3 days back on 7/29 Last pill 08/10/14 SVR+4

 
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