My recent HBV-DNA levels

Just diagnosed or new to the community
1

Hello,

I’m new to this wonderful forum. First of all, I would like to thank everyone who created this space and contributes with their answers. I’m 40 years old. I was first monitored at age 13 due to being HBeAg positive with a high viral load and normal liver enzyme levels.

At age 13-14 i get zeffix and interferon treatment for 4-6 months but it was failed. Hbv relapsed again.

This situation continued until I was 36.

My HBV-DNA remained consistently very high for years, in the range of 10^7 to 10^8 (copy). My AST levels were normal, and my ALT was sometimes slightly below or above the normal limit, but it never exceeded twice the normal value.

In 2019, I started TDF and switched to TAF a year later. The switch was made as a protective decision since I knew I would be on treatment for a long time so i need safety profile antiviral. I have been taking my medication regularly.

Between 2019 and 2025:

(I’m giving values in log10 where applicable)

I have no mutation test for hbv.

Anti-HDV: Negative

HBsAg: Varied between 600–2600–1400; latest value was 1400

HBeAg: Values like 1600–800–400–200; latest was 50

Anti-HBe (positive if below 1): Gradually decreased from 80–40–20; latest was 1.50

HBV-DNA dropped from 180 million IU to around 31 IU and has remained in the 30s for the past 3 years. However, this year I was tested and got 50 IU, and then one week later at another lab it was 78 IU.

FibroScan: 5.6
Albumin: 48 g/L
GGT: 13 U/L
AST: 24
ALT: 23 (Pre-treatment ALT was 40–60)
AFP: 0.91

I’m very upset about the HBV-DNA level. But at the same time, I tell myself, “You lived with extremely high viral loads for years — what more do you expect?” These are the questions running through my mind:

  1. Am I slowly developing resistance to TAF, and could my viral load eventually go back to its old levels? Or could these be clinical or biological variations? For example, could this be related to transitioning from the immune tolerant to immune active phase?

  2. If an additional drug is to be added to my treatment, should it be added alongside TAF, or should I switch back to TDF? I vaguely recall that after switching to TAF, the decrease in HBeAg slowed down — but that might be purely coincidental.

Lastly, when I was 13 years old and visited the pediatric gastroenterology department, I remember seeing a poster on the wall. It said, “Are you aware of Hepatitis B?” It was a black-and-white picture of a happy family — mother, father, children, and a dog. The entire photo was in grayscale, except for one slightly sad-looking child who was painted completely yellow. That image made me feel awful and very alone back then. But now, I can share things with people like you. I just wanted to say that communities like this can mean so much to some of us.

With love. @ThomasTu @john.tavis @availlant @Caraline @Bansah1

1 Like
2

Thanks for sharing @ceng85 and welcome to our community.
Thank you for your kind words. We all each other.
I can’t comment on your results because I’m not a medical expert but someone will soon.
@ThomasTu @Bansah1

You must’ve been pretty frightened to see that picture of that yellow child, being a child yourself. It’s just horrible.

2 Likes
3

Hi @ceng85,
Welcome to the community. To start off, I am glad that you are on treatment now. I think you mentioned that viral load was at 180 million and after 3 years it’s at 78 currently. This is the fantastic work of the current antivirals. 78 is very low that it won’t qualify you for treatment. I wont worry overly about this, given that your AST and ALT are in the normal range. Keep an eye on it. The 3 important tests to focus on are surface antigen, ALT/AST, and viral load. And in this case all of them are looking good.

There is no additional medication to be added. Try and eat healthy, remain in care, limit your stress levels, avoid drinking and smoking, sleep well, exercise and all that good stuff. Keep us posted. Bansah1

1 Like
4

I forgot to add, such fluctuations can happen and it’s not an indication of a mutation. Rather just the immune system and medication working to gain control over the virus.

1 Like
5

Maybe a somewhat related question, but when I first started antiviral therapy, I think my viral load was a little over 10,000. It had been in the tens of millions, but my immune system had started to attack the virus before I started treatment, which brought the levels down a fair amount.

I was on the antivirals (TDF) for 2.5 years, and I reached a detectable < 20 IU/mL result within the first year on treatment. But it never went any lower than this. During that time, I also went through e antigen seroconversion, and my doctor told me that I could try stopping treatment. So I stopped my treatment in 2017, and was not on treatment for five more years after that. Then, in 2022, my liver enzymes and viral load started increasing again. I made an appointment with my hepatologist, and we decided to start me on treatment again. By the time I got in to see him, my viral load was already decreasing. I went from 167,000 to 2500 over the course of 2 months on my own. Then, I got to undetectable HBV DNA within 6 months of being back on treatment. I’m curious why I was never able to achieve and undetectable viral load the first time that I was on treatment.

1 Like
6

I am not a doctor. There is no known resistance to TDF or TAF, according to current research literature. HBVDNA do fluctuate. I think your fluctuation is insignificant, a ten-fold increase is considered to be significant. Your ALT, Fibroscan score, and HBVDNA < 2,000 iu/ml all look good.

1 Like
7

You did achieve hbvdna < 20 iu/ml in your first year of treatment. I believe “undetected” hbvdna result depends on the sensitivity of the hbvdna assay used. Both < 20 iu/ml and undetected are great results.

2 Likes
8

Hi @et5656 and @ceng85,

Thank you both for sharing your experiences and asking your great questions:

Antivirals can potently reduce viral loads by over a million-fold. The very small changes you are seeing are more likely to be fluctuations in the tests, rather than real clinically relevant changes. No cases of TAF resistance have been observed in the clinic as far as I know.

This is terrible - I am sorry that you had to experience that. The hepatitis B foundation, hepatitis B voices Australia, and many other community organizations are dedicated to co-design of messaging and awareness campaigns, so we can minimise these events. We’re still burgeoning, but already making a difference!

As above, the antivirals can reduce it by more than a million-fold, but may not get everything. If you are starting from a higher level, then you may have some residual replication. Despite this, we do not see any resistance to 1st line antiviral therapies. Also, we’re not necessarily sure what form this residual HBV DNA is in: it could be virus, but could also be free-floating viral DNA in the blood.

Hope this helps,
Thomas

2 Likes