hepatitisresearcher

[spcecst2]

Your opinion please? Lets say a patient went thru treatment (1b) pegasys/copegus 180/1200 for 48 weeks, starting VL was 10 mil, middle aged male, slight liver damage, still detectable at 600 week 12, clear week 16 (less than 50), relapsed, waited 3 months and started treatment over, VL 500,000, double dose pegasys 4 weeks, 1400 copegus, no VL detected at week 4 using heptimax, did shot every five days from week 4 thru week 12, did 1600 copegus for month and half, waited full seven days at week 12 and got negative heptimax, doing 180/1200 rest of treatment, ast/alt normal at week 12, does this person have the same chance with RVR statistics (as high as 85% SVR) with 48 weeks, or are those RVR statistics only good for someone who does treatment the first time using the SOC? I hope you can understand what I’m asking here?

[merryBe]

I'm curious as to why they didn't try to suppress your rash with some of the stronger allergy drugs rather than steroids, known to harm the liver?

[Hepatitis Researcher]

You might want to read the explanation on how the HCV specific activated T cells are developed in the recent "vaccine"  thread, where I explain it in the necessary detail, as "laytermy" as possible without loosing it all,  building it up from scatch..

[spcecst2]

You said to whrose ""having developed those magic activated T cells"" I read this  ""Hepatitis C virus (HCV)-specific T cell responses are critical for spontaneous resolution of HCV viremia"" if you have a minute could you explain a couple of things? How does one's body ""develope"" these ""magic activated T cells"" is this what happens (to some) when we are on treatment ((in lay terms please)) and is this ""the negotiation between virus and host immune response that determines SVR"" you spoke of earlier?

[mremeet]

FYI I took large amounts of prednisone starting at about week 7 during my tx (VX950 trial) to control a telaprevir rash. And I took gobs of the stuff for well over a month afterwards, with doses ranging up to 80mg/day (that's a LOT). Then I stopped the VX950 early (by week 8) and was no longer anti-virologically covered afterwards by it (VX950 leaves your body very quickly). Then I stopped taking ribavirin for several days, and then only continued with a reduced dose afterwards (800mg vs 1200mg). And this all happened by about week 8. Then another week later I had to get a jolt of a powerful IV immunosuppressant called solumedrol (much more powerful than prednisone, but in the same steroidal class of drugs). And this all happened between about week 7 and week 12, right smack in the middle of the most critical phase of tx (for SOC anyway). And yet I maintained my UND status during all of this and went on to SVR after 41 weeks of tx (with sub-weight based riba during the remaining tx). As you can see powerful immunosuppressants like prednisone and solumedrol don't even seem to be able to unhinge an SVR, even though I didn't (technically) have my SVR at all yet. I don't know how powerful humira is, or what doses you'll be taking, but I doubt it will have the immunosuppressive power of what I was adminstered. I'd trust your docs on this one. You don't want to take immunosuppressants willy nilly that's for sure, but if I really needed them again I would use them judiciously as required, and would do so without too much fear. From where I stand, if SVR doesn't truly mean complete eradication, it sure puts on a reasonable facsimile thereof.

[Hepatitis Researcher]

A permanent supression/control of remnant virions aftert SVR by an established vigorous Class I and II T cell response tends to be very stable and not very dependent on TNFalpha/unspecific proinflammatory signals. Therefore chances that Humira will cause a HCV breakthough/SVR loss are extremely slim.
With respect to the "occult" "remnant" infection, it has to be clearly stated, that in all likelyhood we are dealing with a huge range of differences within the remaining viral genomes, from close to Zero to many millions, without a simple way to check for that, other than sending a biopsy to Castillo in Spain. What matters its the apparent stability of SVR in almost everyone, regardless where they might be in that range.
Nevertheless your concern is not totally unfounded and only after many years of many SVR  patients on Humira we will know for sure.( Provided someone publishes/collects that data. Not the company that makes Humira, I would assume)

[willing]

you might want to flag mikesimon and discuss his personal experience with the tradeoff between immuno-suppressants  and hcv rebound. I only investigated this briefly but my impression was that among liver-transplant patients rebound of VL in response to the drugs required to prevent rejection is fairly common. The good news for you should be that, having developed those magic activated T cells they'll stay with you for life - reduce the immuno-suppressant dose and the VL should drop to UND.