This is a very good presentation, with audio, regarding reasons, and possible solutions, for null responders to previous SOC and those who have failed new triple tx. It was posted in a previous thread by epicrose. I thought it might be worth bringing to the top. Any thoughts or comments??????
I have copied and pasted the post from epicrose- see below. Thanks epicrose.
http://www.medhelp.org/posts/Hepatitis-C/DID-YOU-HEAR-THE-GOOOOD-NEWS/show/1668577
I failed triple (incivek) Oct 2011. GT 1a. IL28B's CT
I'm now looking to trials. I'm also trying to figure out the reason for my breakthrough on week 12.
There's a great paper discussing resistance. Basically, it states Resistant Associated Variants (RAV's) return to WT depending on their fitness. If they're extremely fit, they'll remain the dominant virus.
Dr. Pawlotsky, author, wrote an HCV resistance paper (attached). He states the two protease inhibitor sub-groups, linear and macrocyclic, are similar chemically and would share extensive cross-resistance.
Pawlotsky's theory is Tx Failures w/Triple Combination with DAA's is caused by insufficient response to IFN, which in turn causes an uncontrolled growth of DAA-resistant HCV variants. He states to prevent Triple Tx failure, he recommends;
1) high dose of IFN/Riba with a protease inhibitor;
2) quad therapy to increase barrier to resistance to DAA's (w/IFN/Riba);
3) an IFN-free therapy with multiple DAA's.
http://74.43.177.57/courses/2010/pg/pawlotsky/player.html
Happy Reading! .