After 16 week with Interferron + Simvastatin

[Otan]

Took 1st dose on 21 Oct 2011 and on 11 Jan 2012 HBV DNA not detected.  
Below is the lab history,                          

Date            13/9  20/10  21/10  11/11  16/11  9/12  15/12  6/1/12  11//1/12
                                   1st dose                                   12th dose
SGOT                    35*                          49*             63*                  67*
SGPT                    63*                          78*             89*                  90*
HBsAg     366.44  255.68                                                              176.4*
HBV DNA2.54x10^5                                                                   no detect

Result on week# 16

SGOT  86
SGPT  130
HBsAg  10.49

When HBsAg became zero, then what to do? Is that time to stimulate Anti-HBs?

[studyforhope]

Here are the countries where zadaxin is approved.


Argentina, Azerbaijan, Bahrain, Brunei, Cambodia, China, Dominican Republic, Hong Kong, India, Indonesia, Kuwait, Kazakhstan, Kyrgyzstan, Laos, Malaysia, Maldives, Malta, Mexico, Moldova, Pakistan, Peru, Philippines, Russia, Singapore, Sri Lanka, Thailand, Ukraine, United Arab Emirates, Uzbekistan, Venezuela, Vietnam
Chronic Hepatitis B
Marketing Approval

[Otan]

Studyforhope, Steff, Cyrus

From 3rd March to 3rd Apr I took Baraclude. Now I have my Viread 4x30 tablets, but not started yet.
Will it good to take Viread while I am in HBV Vaccinasion? Does Viread kill the HBV Vaccin?

FYI, I still cannot find the Zadaxin in Jakarta (indonesia) and Nairobi ( which recenly I visited).

below is my status upodate...



6/7/12 38 dose interferron
12/7/12 SGOT-93 SGPT-142; HBSAG- <0.05 iu/ml; HBSAB-negtv
17/7/12 Start taking Baraclude 0.5mg, 1 tablet per day
20/7/12 40th dose intrfn
25/7/12  GOT-108 SGPT-171
15/8/12  Last Baraclude taken
15/8/12  SGOT 117 SGPT 207; HbsAg- not reactive
24/8/12  HBSAB- 70 mIU/mL
14/9/12  48th dose intrfrn
19/9/12  SGOT-102 SGPT-162; HBV DNA- undetct; HBSAG quanty-
<0.05iu/ml; HBSAB- 122.58mIU/mL
16/10/12  SGOT-88 SGPT-165; HBSAB- 107.13 mIU/mL

6/12/12 SGOT- 34 SGPT-53; HBSAg- non reactive; HBsAb-71.43
10/12/12 Took 1st dose vaccine of Engerix TM-B Adulta dose, r-DNA 1ml HBsAg 20 ug

8/1/13 SGOT-27 SGPT-45; HBSAg-non reactive; HBSAb-52.88
10/1/13 Took 2nd dose of vaccine
22/1/13 HBSAb-43.2
18/2/13 SGOT-25 SGPT-40; HBSAg-non reactive; HBSAb-15.1
----------------------

6/3/13 SGOT-26  SGPT-37; HBV DNA-undtc; HBsAg Qty- <0.05 iu/mL; HBsAb- 26.12; HBeAg- Non React; Anti HBe- React

22/4/13 SGOT-27  SGPT-46; HBsAg- Non React; HBsAb- 20.4

[cyrus131]

Dear Otan,

How are you recently?  Kindly if you could share your updated status, please.  Many thanks.

Regards,

Cyrus

[Otan]

Stef n Studyfh,
Thanks a lot...

[studyforhope]

The fact that no vaccine was used in the replicor zadaxin enhanced patients, can be interpreted such that the adjuvant is the critical component, in this case zadaxin, since small amounts of surface antigen is still present in these patients anyway.
This is not to say that a vaccine would not have driven the resulting titer even higher. But it is also possible that he alum contained in these recombinant vaccines would have had a negative effect on the overall outcome.
We must not forget that while the AB titer can be easily measured, the critical effect operating here , invisible to us, might be a reinduction of the all important TCell response. As a matter of fact, we can be quite sure that the boosting in AB titers that was achieved resulted from a T helper response that stimulated the B cells to produce more antibody.
As such we might see the antibody response as a cheap surrogate marker of a more global TCell response that will include the precious cd8+ cells, that have the capacity to clean and clear more remaining infected cells.

[studyforhope]

Alum is still a necessary ingredient of the prophylactic HBV vaccine. But it promotes what is called a type II TH2) response, where a cytokines mix is induced that does not propel a cytotoxic TCell response. But rather suppresses it. It is more useful for an organism, that is not yet infected with an intracellular parasite, to limit its reaction to the production of infection preventing antibodies. This also effects the subtype of the antibody within the IGg class that will be produced, from strictly neutralizing to cytotoxic.
If you search joerg reimann and reinhold schirmbeck in pubmed you will find wonderful papers on HBV response induction with various of surface plus core plus RNA and adjuvant approaches and the tremendous variation in response they achieved. All in mice, but no one else has done that kind of highest quality analysis on how a therapeutic vaccine could be composed.

At very low levels of surface antigen, AB tend to become visible even in the presence of the unbound antigen. In this case however, just as in the replicor patients without immunoenhancing therapy, the low visible titer is indeed a low titer.
This phenomenon also shows that the kinetic of immuncomplexing by the ABs is somewhat slow, therefore we have free components present.
This is of great significance, since it points to the need of a very high antibody level if the goal is prevention of local intrahepatic reinfection as it exists after seroconversion or after liver transplant.