I think your treatment is effective suppressing VL. Hope soon it will be UND.
It looks to me you started treatment while you are still in immune tolerant stage judging from your ALT level. Is there any reason given to you why u needs treatment at this time? Your data also showed that interferon had dropped the VL from 1.3M to 668IU/ML before you started combo - so you need to monitor yr VL at 12 wks to have further assessment & hope it goes to UND.
I believe that Pete's initial viral load drop was due to interferon treatment which was abandoned as it did not lower his viral load enough. Is that right, Pete?
Things are looking good now...Ann8 has good advice.
If it were to go to UND what would the results be and what would that actually mean? From what i think, it sounds like the vius would then be dormant but not gone.... Which is ideal if it were not for the fact that later on in life it could suddenly become so aggressive it wouldn't be controllable... Is this correct?
When it goes UND and keeps UND, you become inactive carrier:
"Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy [3,4]. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC) [40-42]. Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state [40-43]. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up [29,33,34,40]."
The treatment end-point for you will be to force SVR which will be manifest by low DNA VL < 300 with normal ALT and e antigen loss. This will reduce the liver injury. Since you started your treatment during immune tolerant phase (not ideal) and hopefully you could push it through fast and lost the antigen. This is where drug effective & resistance managment become important. Selecting high potency and high resistance antiviral is improtane to start with....Baraclude+Tenofovir. The current treatment protocol is to have + antigen sero-convert to -ve antigen and continue antiviral medication for another year before stopping....The relapse was estimated to be in the 20-30% range for +ve entigen pts.
>> Which is ideal if it were not for the fact that later on in life it could suddenly become so aggressive it wouldn't be controllable... Is this correct?
Hopefully they will have a cure to it by that time.....you are going to take a long time before reaching uncontrollable stage. The key is to manage drug resistance.