I do disagree with your doctor the picture is pretty clear for immune activation and clearance
low hbsag
low hbvdna (9000iu/ml is not high different guidelines consider low/inactive 2000 (europe) or even 10.000-20.000iu ml some others guidelines
relevant fibrosis or inflammation from cytoxic clearance of infected cells
i do think that peg mono might easily work, but in the meantime see if you can apply dr coimbra protocol and then if hbsag and hbvdna go down.i do think that those with a doctor willing to monitor serum and urine calcium might try this and see the effect on hbsag hbvdna
That is the hard part my fibrosis is at 7.6 kpa and will repeat it next month and I'm still on no medication until probably next March when the Doctor will have a clear picture. What confuse me is I have a low hbsag 220 iu/ml but high viral load which is 9000 iu/ml so confused of my status if i'm a carrier or slightly active like my doctor describe
I dont think the genotype dependent hcc studies are very reliable except for geno c but just my opinion
i think more than genotype it is important to keep fibrosis at less than 5kpa and liver inflammation as low as possible whatever the genotype
Just curious guys any comments from the expert members on genotype D?
But when you say higher chance to cirrhosis isn't that also higher to HCC?
That's a good question, Mike. The conversation that I had with my doctor was that it was Genotype C that had a higher risk for HCC, Genotype A & were easily treatable (and he said he's helped cure them too in the past). From the understanding that I have on this board with some, Genotype D was higher chance for cirrhosis.
I'm sure someone else can chime if if they want and have more facts. I'm just going on what I remember was told to me.
I have a question on all these research but I get different answers:
1) some research from 2014 say genotype C and D have higher cirrhosis and HCC while other research from 2013 say genotype A and D have less chance to develop HCC
So which one is true on genotype D?