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trial: hbsag clearance after 4ys hbvdna und and stopping tdf

http://clinicaltrials.gov/ct2/show/NCT01320943

it is possible that stable nucs therapy with potent tdf or etv rescue immune response after many years or that the alt flare due to tdf stop makes cccdna unstable and clears hbv, very interesting trial

one thing is certain normal ast/alt make cccdna very stable and abnormal alt are needed to lower hbsag and cccdna fast
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Avatar universal
Guys,

But what happens if you have a mutant infection like I do?

HBV Genotype A
Basal Core Promoter Nucleotide - T1762/A1764 Mutant
PreCore Codon 28 - Wild type

I have stopped baraclude after 5 years. My Hepatologist was was waiting for that flare. VL went up to 100,000 copies and my AST and ALT stayed normal. I decided not to take a chance and went back on baraclude.

I also want to do PEG because these nucs are just a waste of time.
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Avatar universal

alcool is definitely out of the question the damage needs to come from our immune system and not toxic substances, alcool destroys immune cells too.i dont mean to offend the chinese forum guy but using alcool is a little bit foolish
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Avatar universal
LOL - they are many way to destroy liver cells.

Indeed is you find why / how the HbsAg decline we can have a better answer to our quest. (in patient 4318 the HbsAg kinetics look to be  independently by TNf, or by ALT or  HVB DNA or other visible marker)
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Avatar universal
with Patient 4318, I think (my guess) he/she just stopped taking TNF. It was not planned. All the patients who lost HbsAg, all have continuous decline of HbsAg levels - why?

You are right about using drinking to kill liver cells. How can you control how many cells to kill and which ones with drinking? A reader replied that you can also achieve the damage by taking out your liver, cook it a bit, and put it back (LOL)
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Avatar universal
Patient 4318 is realy interesting and the protocol for this patient was designed with a off drug period, so I wandering what was the theoretical reason for the dr. to try such a approach. (I was under the impression that stooping a antiviral include the risk of mutation - so do to this reason no one will design a schem using a off drug period). Another observation was that the AgHBs of this patient was decreasing also during the falare, so I suppose that some other relation can exist.

Regarding the suggestion from the Chine forum member (regarding the alcohol consumption) the ideea have a point, but is hard to target the cells that have ccDNA (or all the cells have ccDNA? ). Anyway until I found out that i have HVB infection I was a social drinker and use to drink weekly and my test results were relay - but this not means that we should have start to drink even if some dr. mentioned that in case of a inactive carier limited social drinking is ok.

interferon on a flare can be dangerous, but if is made by a good doctor and the dose is adjust properly this can be a option.
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Avatar universal
This is what the clinical trial said. You may or may not get a flare (ALT or  hbv dna), if you do have a flare, it may be damaging or self-limiting. Lots of possibilities, sure hope we can get some answers.

"Withdrawal of antiviral therapy can result in hepatic or alanine aminotransferase (ALT) flares as Hepatitis B Virus (HBV) replication resumes; however, in some patients, a flare exacerbates chronic hepatitis temporarily but can also result in viral clearance. Hepatic flares are common after stopping anti-HBV therapy.

Only patients who already are on treatment with tenofovir disoproxil fumarate (TDF) for at least 4 years and who achieved and maintained virologic suppression (< 400 copies/mL) for 3.5 or more years will be included in this study. One treatment arm will stop the TDF therapy while the other treatment arm will continue the TDF therapy.

Patients who stop TDF (Arm A) will be monitored very closely with special focus on biochemical flares (especially ALT increases) and virological relapses (Hepatitis B viral load increases). If any subject in the stop therapy arm exceeds one or more predefined limits for such flares or relapses, TDF will be reinstituted.

The study will assess Hepatitis B surface antigen (HBsAg) loss (i.e. specific Hepatitis B virus components are no longer detectable) and seroconversion (occurrence of Hepatitis B surface antibody, a specific antibody which usually occurs after HBsAg loss) rates during study duration. The percentage of patients who need to restart TDF therapy in the stop arm will also be evaluated."
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