I just saw your reply
Thank you
Hepatitis D can coexist with HBV. I've had it tested and it is pretty routine if you are HBV positive, especially if both are fairly common in your country.
It used to be that attaining HbeAg negative and HbeAb positive was a good thing but then they found that some still have high viral load and much damage, which Stef mentioned due to mutations that still produce HbeAg and create that e negative HBV. Now, we know that as long as you have HbeAg negative, HbeAb positive, no or low viral load which is less than 2000 iu/ml, normal alt, most would agree you are in the inactive stage. If you can track quantitative hbsag you will have an even better idea if you are inactive or not.
Be sure to monitor HbeAg, viral load, alt because you can revert back to HbeAg positive, you can go from inactive to e antigen HBV (active), or you can stay in the inactive stage. HBV is sneaky and over time your status can change. Hopefully you are in the inactive stage and stay that way. In the inactive stage still monitor with labs and scans, because we still have that HCC and cirrhosis risk, although lower in the true inactive stage.
A kind gentlemen just has explained the result to me and after read this website http://www.hepb.org/patients/additional_blood_tests.htm one again I think I still got it.
HBeAb or anti-HBe (Hepatitis B e-Antibody) - This antibody is made in response to the e-antigen and is detected in patients who have recovered from hepatitis B infections as well as those who are chronically infected. Chronically infected individuals who stop producing e-antigen sometimes produce e-antibodies. The clinical significance of this result is unclear but it is generally considered to be a good thing. In rare cases, anti-HBe may be associated with active viral replication in patients with e-antigen negative virus mutations.
Oh yeah i was very tired when I read that.
Thats why i mention "typical life cycle"
Congrats as in hbeag neg and hbeab positive.
But thats why i asked for the rest of the stats
sara just said she got E antibody, she got hbeag negative, not a great news because it means nothing in terms of improvement or clearance of infection
most of the time is a worsening with precore or bcp if this happens without therapy (nucs or peg)
Can you share with us Sara how did you clear the virus? Like the way needadvicewithhelp mentioned. Thanks!
Congrats
Bearing in mind the typical life cycle of the virus.
Also did you get your other stats checked hbsag, hbsab, ALT, AST??
I was infected from birth and just a few days before Chrismas I got a report from hospital confirming that I now got E antibody positive after e antigen negative for a few years. I still can not believe this. I'm asking for another blood test just in case it was an error somewhere in the process.
Heres a link with information
http://hivinsite.ucsf.edu/insite?page=hmq-1305-01
Hey, I don't know what TAF means? Can you explain for me?
Thank you
of course, HBsAg neg = much less virus (close to zero) = much less mutation chances
Thanks
Obviously being geno type C with mutations is riskier.
But HBSAG 'Non Reactive" reduces the chances of mutations?
Even with a pos antibody level, there will be remnant virions produced in the liver.
HCC risk will be reduced if precursor clones are diminished, which typically produce hbsag - not always virions in case of integrated hbv sequences.
But a pos antibody is a strong sign that the remaining hbsag production from all these sources is minute.
Hi Studyforhope thanks
"The undetectable status of the pcr blood test DOES NOT MEAN that no more virus is produced in the liver. It means that the small remnant amount is absorbed and internalized mostly directly in the liver"
So in regards to the above comments even if hbsab are produced does it mean there is still remnants absorbed into the liver?
But would I be right in assuming it dramatically reduces the chances of HCC with hbsab rather than without? like a resolved acute infection for example?
We cannot say at this point if TAF or TDF is more potent in the induction of a hbsag loss.There are good reasons to think that TAF is more potent in the hbv replication inhibition in the liver.
Both substances are just chemical precursors that have to undergo critical transport processes, stability issues while en route to the hepatocyte cytosol and enzyme mediated processing to the final metabolite that enacts the actual inhibitory action on the hbv polymerase :TENOFOVIR DIPHOSPHATE.
NakedTenofovir itself can barely enter the liver cell and is therefore almost completely filtered away in the kidney glomerula, where HOWEVER it is afterwards actively absorbed into the proximal tubuli by a special transport mechanism unique to these cells. That is the reason for its accumulation in the tubuli cells with the resultant toxicity for the kidneys.
Tenofovir disiproxil fumarate, the actual chemical in the viread pill is absorbed in the intestine at a decent about 50% efficacy.
When it enters the bloodstream and reaches the liver via the portal vein, it immediately starts to fall apart with a fairly short time constant, slow enough thankfully that a small portion of INTACT TDF will touch the liver cells and then be absorbed to the inside, where it's further processing via 3 steps to TENOFOVIR DIPHOSPHATE will start.
All the other TDF will dissociate into naked TENOFOVIR that cannot enter the liver and is eliminated in the kidney.
TAF is fundamentally different in its pharmokinetic behaviour in that it is STABLE in the blood stream and will enter the the liver and other organs with ease, LEADING MOST LIKELY TO A SUBSTANTIALLY HIGHER intracellular concentration in the hepatocytes and after the 3 further processing steps will achieve a HIGHER FINAL CONCENTRATION OF TENOFOVIR DIPHOSPHATE in the cell, with a higher inhibition of the hbv polymerase and a resulting slowdown in the remaining synthesis of new hbv dna and virions.
The problem with all antivirals is that the synthesis inhibition is not truly complete, leading to a much slower but ongoing reinfection, therefore no cure, no true dry up op virus production.
The undetectable status of the pcr blood test DOES NOT MEAN that no more virus is produced in the liver. It means that the small remnant amount is absorbed and internalized mostly directly in the liver.
In summary, it is possible that TAF leads to substantially higher TENOFOVIR DIPHOSPHATE concentrations in the liver, despite its dramatically reduced dose of 25mg vs 300mg, which might further result in a smaller remnant virion production and consecutive reinfection of neighboring liver cells so that immune mechanisms operating simultaneously might have a higher chance of catching up and reducing the total amount of infected liver cells better than TDF.
But I have to say "MIGHT" because we cannot directly measure these metabolites and infected cell numbers in a human trial. All we can do is follow surrogate markers like serum hbv dna and hbsag.
It is also possible that the potent advantages of TAF over TDF are mainly lost due to the dramatic dose reduction.
What is quite certain however is that a huge reduction in the kidney burden by NAKED TENOFOVIR will occur with the small TAF dose, and that would in itself be progress towards the kidney and bone problems that , to a small but obvious degree are burdening the long term use OF TDF in some patients.
Stef whats your thoughts on the vit d supplement i posted the link for?
it is just coincidence taf like all other nucs will keep same low hbsag loss close to 0-1% for hbeag neg.
hbeag pos on tdf gets 16% hbsag loss by 3 years so maybe taf will improve this a little but very unlikely for hbeag neg
Thankyou my friend.
Yes agreed its a blessing that im eternally grateful for :)
Makes me speculate a little thinking if you are on tdf and then they make the switch to TAF could the same happen hbsag loss happen for you? We live in interesting times :)
Hey there! I am Genotype D, which is primarily dominate in the European countries (though I am in the USA). Most Genotype C are of Asian culture, so yes yours is a bit rare to see but it does happen. Genotype C is also the highest risk of HCC from what I understand. What has happened to you is a blessing!! Keep up the excellent work!
From air Haha that actually sounds funny. :)
It seems a bit difficult to quantify as its liquid.
Stef did look you at the link i posted with the vit d supplement i was using?
My vit d levels were very high i was told by the doxs. I'll get the exact numbers on my next appointment and post them.
But its funny when i used vit d a did feel alot more energized
definitely not getting vit d from that supplement, you get more from thin air that from 700iu
mushrooms are rich of vit d2 it could be from there and from the fact you were clearing hbv but levels for immune boosting are 80-100ng/ml i dont think you reached it
The sun? No way im in the uk.
My diet has has alot of mushrooms oily fatty fishes etc
My vit d levels are high aswell
Oh yeah I wouldnt be suprised re taking the NUCS nor would I mind im just praying for anti bodies now
Well im caucasian and geni type c my doc said im the first they met with that profile.
From what i understand geno type is the most vulnerable yet the most aggressive.
Lucky what geno type are yoy?