Welcome @A7xImpulse
Thanks for joining us and sharing your story.
You have some great questions there.
Unfortunately I can’t answer them but our
professional team will be with you soon.
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Dear @staystrong,
With such a low HBsAg, you are actually close to a functional cure and this may actually improve over time. 391 IU/mL is still a very low viral titer.
Any idea how long you have had the infection (or failing that the date of your original diagnosis)?
Two options to consider are:
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Monitor qHBsAg every 6 months for the next year and see of you actually get to HBsAg loss. Here I would also expect HBV DNA to also continually decline.
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Start antiviral therapy anyways and also look for HBsAg loss. If you reach HBsAg loss with two consecutive tests 6 months apart, current guidelines indicate stopping therapy becuase functional cure has been achieved.
Thank you Availlant for your response. I have been diagnosed back in 2008. I think I got Hep B from dental work but not sure may be back in mid 90 or early twenties.
So in my case would you recommend taking Velmidy 25 mg or Entecavir 0.5mg?
Dear @staystrong ,
Both of these medicines will be highly effective in suppressing HBV replication. Entecavir will be off patent so if you have to pay for your medication this may be a preferred option. TDF is also off patent and is very safe and effective. Vemlidy is also a very good medicine but still under patent protection (and so the most expensive). Vemlidy is used primary in those small fraction of patients who suffer from reduced kidney function or bone demineralization with long term therapy.
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Dear @A7xImpulse,
Thanks for sharing your story and these are some great questions that the research community are actively working on.
For anti-HBc, it does not appear to do anything for fighting off an infection (though happy for any immunologists @mat @nina.le.bert @Greg to confirm, deny, or correct this). The likely cause of this is that infected cells continue to secrete HBc (or viral capsids) that continue to stimulate the immune response.
Regarding low levels of anti-HBs response, this may be a function of the test (it may cross react with other antibodies), or indeed reflect the small amount that is produced and then immediately bound to the circulating virus/subviral particles.
Regarding immune response recovery, good question, I don’t really know, and would appreciate the help of some immunologists or a more capable @ScienceExperts in this field.
Hope some of this helps,
Thomas
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Thanks Availlant for your response and guidance.
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Thank you Thomas for your response,
“For anti-HBc, it does not appear to do anything for fighting off an infection (though happy for any immunologists @mat @nina.le.bert @Greg to confirm, deny, or correct this). The likely cause of this is that infected cells continue to secrete HBc (or viral capsids) that continue to stimulate the immune response.”
Wow, I didn’t know that just capsid proteins (without surface envelope) also get secreted out of infected hepatocytes. That would explain why our bodies keep producing anti-HBc.
I found out from somewhere that the majorities of HBVs assembled does not actually contain any viral DNA. Are these virus without viral DNA classifed as sub-viral particals? Is HBe antigen related to these “empty” HBVs? Or is HBe antigen something completely different, with a different surface protein makeup.
Thanks for reaching out and answering my questions!
Hi @A7xImpulse,
Yes, the virus produces a lot of different proteins and structure including the infectious virus.
These include:
#1) Infectious virus, with surface, capsid, and DNA
#2) Surface protein with capsid, but no DNA (10 times more common than #1)
#3) Surface antigen alone (10000 times more common than #1)
This is one aspect of why anti-HBs is not generated in sufficient quantities to detect: there’s just so much HBsAg (surface protein) that it just gets swamped out.
HBeAg as we define in in these terms is its own entity. While some of the antibodies that recognise HBeAg also recognise capsids (HBc), HBeAg and HBcAg have quite different structures.
Hope this helps,
Thomas
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Hi everyone…am lily, am so grateful to be here, am still reading through, getting to know everyone and learning from the experts.
Unfortunately, my request for HDV blood panels etc. has not been granted. Not an encouraging sign, and yet another stressor. It also impairs decision making regarding medication by reducing diagnostic information. So, I have some (probably naive) follow up questions.
From your reply to EH1999 (May 2022), is viral load a measure of what is in every blood cell circulating in the body? (Again, my old brain is not reading closely enough/retaining. I see, it’s per ml of blood, not every blood cell.)
Can an antiviral achieve a functional cure, and if so, does it rid the blood stream of all virus plus SVP’s? Would that apply to a spontaneous functional cure? (I did not catch the implications of part of the reply to Aman, 16 Feb “Unfortunately, these drugs do not target the production of HBsAg, which is why they are life-long therapies” before posting.) However, in a functional cure, is all the virus/HBsAg and are all SVP’s removed?
Can it be determined from a Fibroscan score of 19.4kPa and CAP score of 266 dB/m what percentage of the liver has been damaged by fibrosis/cirrhosis?
With regard to the reversibility of fibrosis/cirrhosis, some sources suggest it’s reversible, particularly in reference to alcohol-induced hepatitis and steatotic liver disease, other sources say it’s not. Which is true and, either way, would it apply to cirrhosis in general; in other words, is cirrhosis cirrhosis, regardless of cause?
Thanks again for any insights.
Welcome @Lilibet94. Take your time to read around and if you have a question(s) please don’t hesitate to ask. Thanks, Bansah1.
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Dear @Karp ,
See below in bold my replies:
From your reply to EH1999 (May 2022), is viral load a measure of what is in every blood cell circulating in the body? (Again, my old brain is not reading closely enough/retaining. I see, it’s per ml of blood, not every blood cell.)
In HBV infection, viral load (HBV DNA) is an aggregate measure of the replicative activity of HBV in the liver (there is very little replication of HBV outside the liver). HBV infection is not uniform in the liver; some liver cells are infected and produce virus and some liver cells are not infected.
Can an antiviral achieve a functional cure, and if so, does it rid the blood stream of all virus plus SVP’s? Would that apply to a spontaneous functional cure? (I did not catch the implications of part of the reply to Aman, 16 Feb “Unfortunately, these drugs do not target the production of HBsAg, which is why they are life-long therapies” before posting.) However, in a functional cure, is all the virus/HBsAg and are all SVP’s removed?
With approved antivirals, functional cure is rare. However, functional cure is achieved when production of SVPs by the liver is low enough that HBsAg cannot be detected by the assays in use (this is low enough that immune control remains constant). This is also the same with spontaneous functional cure.
It is important to note that with functional cure, inactive reservoirs of infection (cccDNA) are still present but persistently controlled. These can reactivate under conditions of severe immunosuppression (i.e. when taking immunosuppressive medication for autoimmune disorders or organ transplant).
Can it be determined from a Fibroscan score of 19.4kPa and CAP score of 266 dB/m what percentage of the liver has been damaged by fibrosis/cirrhosis?
No, these are aggregate measures of average liver condition. More detailed analysis of liver damage requires a liver biopsy.
With regard to the reversibility of fibrosis/cirrhosis, some sources suggest it’s reversible, particularly in reference to alcohol-induced hepatitis and steatotic liver disease, other sources say it’s not. Which is true and, either way, would it apply to cirrhosis in general; in other words, is cirrhosis cirrhosis, regardless of cause?
Fibrosis can be reversed but this usually occurs slowly (over several years) and only if the source of liver inflammation is removed. Reversal of fibrosis can also occur with effective suppression of HBV infection and following functional cure. Cirrhosis is a much more serious condition where significant structural alterations in liver tissue occur. In some cases, reduction of liver inflammation in cirrhosis can improve overall liver function but cirrhosis can persist (but in a more manageable form). Reversal of cirrhosis and its structural alterations does not frequently occur and when it does, this reversal is much slower than the reversal of fibrosis.
Thanks again for any insights.
[/quote]
Welcome @Lilibet94
Thanks for joining. There is definitely lots to read.
Any questions don’t hesitate. Someone is never far away.
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Dear @availlant
Thank you so much for taking the time to reply, and so quickly! It’s evident that there is so much I don’t understand of this complex process. I really do appreciate what you do and your contribution to this support group. I doubt I’d have any hope of understanding this condition without you and all the other kind contributors, lay and expert alike. I hope my simplistic questions don’t make it too tiresome for you all because I might always have some follow-ups.
“In HBV infection, viral load (HBV DNA) is an aggregate measure of the replicative activity of HBV in the liver (there is very little replication of HBV outside the liver). HBV infection is not uniform in the liver; some liver cells are infected and produce virus and some liver cells are not infected.”
Does this mean that viral load in the liver is measured by other indicators like HBsAg in serum and not by HBV DNA itself (or very little of it)? Until now, I assumed that HBV DNA was actually circulating throughout the blood stream. Given that I also have bradyarrhymia, I’ve been concerned about hepatic/coronary interactions that apparently happen in both directions.
Again, thank you.
Thanks so much…am happy to have found a family
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Thank you…yesss alot to read but am taking it day by day…its comforting to have some one to talk too …
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Good every one my name is jay I just did a full blood test and I was diagnosed of hep b chronic I’m so scared right now I don’t know what to do I live in Ireland but I have an appointment to see a specialist on the 5th of march I’m scared right now and my family is back in Nigeria I’m scared of them as well because I feel I have also exposure my wife and son to this I planned a beautiful family but this now as taken away my joy I don’t know what do I am glad I found this platform I need advice because I’m scared of my family losing them and even my self anytime I see my son picture I just want to end my life this my test result below can some one explain this to me I’m so tired
HBsAg(Architect) positive
Anti-HCV(Architect) negative
T.pallidum Total (Architect) negative
HCV Ag(Architect) negative
Anti-HBe(Architect) positive
HBeAg(Architect) negative
Anti-HBc lgM (Architect) negative
Anti-Hbc total positive
Anti-HDV total (liaison)negative
Please can some explain this to me my heart is so heavy I feel my life counting by the day
Hi @Jay,
I hear you. Don’t lose hope. With this virus, if you take care of yourself by being frequently monitored by a provider, getting your lab work and imaging done each year this virus is manageable. This should not be the end of your life as you perceive or feel. There are many hepatitis B patients who have lived with this virus for many decades and are still doing fine. Think of this virus as having any other chronic disease like high blood pressure that requires long term management. For your wife, children and other family members, have them all tested and if negative make sure they get vaccinated as soon as they can.
Your results confirms that you have hepatitis B, but no evidence of HCV or HDV.
I hope this helps some, Bansah1.
Dear @Karp ,
HBV DNA is present in the virus that is circulating in your blood. Since the HBV virus is produced in the liver, the level of HBV DNA in your blood is an indirect indicator of the overall activity of viral replication in your liver. HBV DNA levels in the blood cannot tell us how many cells in the liver are infected as HBV DNA levels in the blood are a product of the number of cells producing virus and the rate at which these individuals cells are producing the virus.
HBsAg is not a measure of viral replication. HBsAg is almost entirely derived from non-infectious subviral particles which are produced by a distinct mechanism inside infected cells. They are also produced in a subset of infected cells which cannot produce virus.