Certainly - in some cases. And the same thing can be said about PegIntron.

A key reason this can ever happen is that Interferon does not directly attack
the HCV virus. What it does is put parts of the immune system into overdrive -
the parts that recognize and attack the virus while keeping it from
multiplying.

The problem often is the immune system response - which varies from person to
person - isn't complete enough, quick enough, to keep the virus from mutating.
And once the virus has mutated it's far more difficult - if not improbable -
for the same immune system to even recognize the virus, never mind kill it,
any longer.

Finally, and ironically, it's been fairly well documented that the virus, once
it is no longer under the immune system's antiviral siege, will revert back to
its "wild type" RNA coding, leaving it vulnerable to another course of therapy
(at least in the beginning, again). So a second round of tx could again cause
a precipitous, initial drop in viral load - and even lead to SVR (or, if not
complete enough, quick enough, it'll mutate again and the load will rebound
again).

If there was an agent that *directly* recognized and killed the virus, I
suspect the above paradigm could be eliminated - the variables would certainly
be reduced, as the quirks of individuals' immune system genetics would be
pretty much taken out of the equation. Until that time, at least, there will
continue to be treatment failures.

Cheers - and Good Luck with the third round, John. You're one brave
sonofabeyotch for taking it on, but I certainly understand why you wanted to
give it a try, even if your doc might have seemed reluctant...

/greyhackles