Just got my genotype result back...

[itac]

See photo attached.

Can someone explain what does BCP mutations mean?
Also, is this genotype considered better to treat or more chances to seroconvert?
Where is the origin of D in the world?

Thanks!

[stef2011]

we will have a better picture of hbsag decline at 24 weeks but i think that add on can decline hbsag but when baseline is so high we have little lucky to clear hbsag, maybe keeping peg for 2 years if sides are not too heavy

[stef2011]

that s about 13 weeks on peg add on, i know from the add on trial in italy for genotype D mainly that hbsag first go up and starts decline after 3-6months so it looks like you are responding as they found on trials

i d suggest adding gcmaf if you can have it and checking intact pth, vitd25oh is not good to tell vit d sufficiency we usually have problems wtih vit d receptors and only pth will tell you if vit d could bind receptors and get to cells

i also thing etv was not potent enough for you but i guess too late to change it to tdf

are you having sides from peg?

[Raj185]

I started my pegintf therapy from 3/3/15.

[Raj185]

Hi Studyforhope, Stef

I'm chronic HBV patient and have been on entacavir for almost 4 years now since 2011. My HBV DNA was undetected from more than a year now and also my ALT and AST were high since 1 year.

Recently my doctor suggested we can try entacavir + pegintf for 12 weeks, so i went ahead with his suggestion.

HBsAg Quantitative(CMIA)
26/12/14 - 34268 IU/ml
20/02/15 - 16066 IU/ml
03/03/15 -  27602 IU/ml
08/04/15 -  31029.85IU/ml
07/05/15 -  29542.08IU/ml
03/06/15 -  12131.10 IU/ml

my AST and ALT were 64 U/L and  104 U/L  and I got them tested today they are around 130 U/L and 248 U/L respectively.

The only change that I did  between 18/5/15 and today is, I have been taking 10000 IU of vit d3. Otherwise my vitd3 was 29.35 ng/ml on 18/5/15.

I feel there is lot of inflammation in my liver, is this normal with peg intf.

Also my last reading of HBsAg has changed drastically, similar situation happened during feb reading also (see above). I have been doing the test with the same lab and with same methodology.

I also got my HBV DNA quantitative results today, it is around  86 IU/ml.

my worried about the AST and ALT reaching almost 4X the upper limit. Do i need to be worried about it or is it normal.

[studyforhope]

i dont know enough about the micro RNA test to judge whether it is just a formally associated marker of anti hbv activity or if a more detailed understanding of the reasons for this relation is already available.
To discover a relationship with vitD /gcmaf they would have to serially follow you in the on or off phases and then possibly see a relationship.

[studyforhope]

A low viral load and a low hbsag are both signs of reduced presence or activity of viral replication and production of its proteins.

Both dna production and hbsag start from the number of cccDNA, so in principle they go roughly parallel.
But the replication is a complex multistage process that can be hindered by intracellular mechanisms in a different way than the reduction of hbsag transcription.
Consider the hugely different amounts of hbv proteins produced for:
surface antigen
M protein
L protein,
e antigen
core protein
polymerase protein
X protein.
They all are made by transcription from the same cccDNA template, but the initiation of this process is vastly different and its firstly genetic factors in the promotor regions of these HBV genes that determine activity and amount of message produced. Then epigenetic factors, interactions of nuclear DNA associated proteins with the template play a major role in determining transcription speed of all these messages.
For the replication, the pregenomic RNA is formed from the same template, again at a rate that is  quite different.

And the immune mechanisms acting intracellularly, initiated mostly be cytokine receptors and guided through signaling cascades down to the nucleus, can act divergent on the various processes at work in this context.

Thus, we can see quite a divergence between hbsag and viral load, even in the absence of antivirals in a particular patient.