so if the quasi-species may already be in place, is that a separate issue from other ones developing during tx? Are we then possibly faced with both scenarios affecting SVR?
Actually, I read a transcript of Dr. Schiffman testifying before the FDA about Pegasys. He stated that peginterferon does not create IFN-resistant quasispecies. Apparently, these factors are already in place before we even begin tx, especially in geno 1b. There are two 1b amino acid switches that may be predictors of nonresponse, and may be the reason why 1b is a little tougher to clear.
I´m positiv I heard 1a is a little bit tuffer to treat.
Think we have discussed this before here at the forum, some said as you 1b and others 1a and there were studys presented dont have them but if someone have please chime in on this one.
Hey Mk, Nice to see you hear. Very interesting posts. Thanks for posting them.
comeagian: I have always read that 1b is harder to treat then 1a
Hey copyman, great to see you, too. Thanks for the hello.
comeagain: geno 1b nonresponders, or a majority of 1bs, are often the first group to be enrolled in clinical trials, because 1b is the slightly worse of the two, perhaps partly because it tends to inflict more damage to the mitochondria of liver cells. Also, nonresponse can be predicted in 1b patients who carry either of two specific switches of amino acids.
And of course, I posted the exact same thing twice. As usual, my brain is dysfunctional. Excuse the repeat.