When to discontinue chronic hep b treatment

Hi Kinoti,

Just a small clarification for the people watching this thread.

NUCs are not broken down in the kidney, but they are eliminated from the body in the urine. The kidneys drive this process by removal (filtration) of NUCs from the blood. The movement of NUCs from the filtration apparatus of the kidney into the urine is occurring at a constant rate which is independent of the NUC dose.

In rare cases, the active dose of certain NUCs (ETV and TDF NOT TAF) required for effective suppression of HBV infection can lead to an accumulation of these NUCs in the kidney which alters kidney function. This alteration of kidney function can be effectively managed by dose reduction of these NUCs under the supervision of a qualified physician. This dose reduction allows the movement of these NUCs from the kidney to the urine to catch up and lower kidney concentrations, restoring normal kidney function. There is no evidence of actual damage to the kidney with these NUCs.

Best regards,


Please, does these drugs later come back to hunt the kidney? I’ve been seeing people talk about kidney now. Please, it’s unclear, could you please explain.


Dear @Adedeji_Joseph,

As mentioned by @availlant in the above post, change in kidney function is very rare. It is also easily managed by switching medications or altering dosage before any damage actually occurs. The drugs used for HBV (such as entecavir and tenofovir) are very safe. I myself have taken tenofovir every day for many years and have had no trouble with it so far.

Hope this helps,


2 posts were split to a new topic: Navigating the forum

Hi catcher 007
I too have high cholesterol. I tried everything to lower my cholesterol unsuccessfully.
My doctor said high cholesterol can be hereditary. So, I take a tablet daily to lower the chance of a heart attack.
I also take an antiviral because I have HBV.
I do not want to get liver cancer.
If your liver is ok it doesn’t need a rest from one tablet a day. That tablet is a life saver. It’s stopping liver cancer and death.
Specially since liver cancer runs in the family.
Many people have stopped taking their one tablet a day, maybe they aren’t around to reply to you, dead, or are too sick.
I am very grateful this medication is available otherwise I probably would be dead or laying in hospital waiting for a liver transplant.
I hope you find some peace
And keep us informed


Thaks,family. This discussion makes me lose the the fear i I had over starting my medication just incase am initiated to it. I will always consider this as “MY MEDICATION MY LIVER”. Thanks to the brains behind this forum.

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@Opa I’m very happy to hear that news, treatment of other illnesses can be far more traumatic than taking one tablet a day.
I am grateful our medicine doesn’t disrupt my life.


Hello! I’m new to the group. I know about my condition 11 years, I’m 33 years old now. I found out when I was pregnant with my first child. I probably got it when I had a surgery when I was a baby. Can you share how long have you been on medication and if they have to switch you to different one. Thank you!

FYI, When Can Hepatitis B Patients Stop Taking Antivirals? Experts Finally Have Some Answers - Hepatitis B Foundation

So after reading some posts here, If you stop taking medicine, maybe monitor the parameters (alt, ast, viral load etc) every 3 months, yes blood measurement work is expensive, every month would be good if u have the finances. If viral load increases start taking medicine again, idk ?

Some facts:
-Liver cell replaces itself every 200-400 days, I assume that a infected liver cell when it replicates it will not copy the cccDNA in the new liver cell, so the new cell will be clean untill it gets infected by an hepb virus.
-Hepb drugs resistance to tenovofir is very rare
-Immune system attacks infected liver cells, so after killing the liver cell I assume less virus are being created because infected livercell is dead, but this does leaves scaring. Killed liver cells causes high alt and ast.

Because of these facts, I think you can start and stop treatment anytime without causing drug resistance. HIV virus is a different case, I have heard there you cannot stop because the virus mutates differently than HBV.

If we take tenovofir, virus replication is suppressed, so less virus being created, that means less liver cells are getting infected, liver cells replace themselves with clean liver cells, so this decreases virus production also.

Thing is the immune system tries to fight the virus but it gets distracted by virus particles, https://www.youtube.com/watch?v=Iq5nFg-H0xo

Maybe start another thread for this question ? Can hepb virus ever become resistent to tenofovir ? if you take the medicine, when viral load low or undetectable you stop taking it and than when the virus appears you take it again, repeating this cycle, will it make hepb drug resistant to tenofovir ?

Dear @hepb1,

We have to be careful about generalizing some of these concepts to HBV.

While it is true that the liver is one of those special organs which can regenerate itself, we know that the state of liver inflammation in chronic HBV infection impairs this regeneration (which is one of the reasons why fibrosis progresses and can develop into cirrhosis).

Also, while cccDNA is not efficiently sorted to daughter cells during cell division like chromosomes (cccDNA minichromosomes do not contain a centromere), cccDNA does get partioned into daugher cells. As such, even with cell division, cccDNA only experiences a slow decline. Complicating this is the fact that only one copy of cccDNA is required to activate HBV infection. We know this from studies in which people who had been previously infected but achieved functional cure on their own (no detectable viral markers in the blood), reactivated HBV infection when they took immunosuppressive therapy for some other reason (like cancer or organ transplant). This HBV reactivation takes place by reactivation of latent cccDNA which has remained hidden for many years in the liver of the patient.

cccDNA decline on TDF does occur but the rate of decline suggests that the time to achieve “no detectable cccDNA” would be several decades and even then latent cccDNA would still remain. This form of cccDNA is impervious to innate immunity and generates no viral markers.


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Dear @hepb1,

We have seen clinically that starting and stopping treatment can be risky in many contexts and noone should be regularly and repeatedly doing this. While tenofovir resistance has not yet been described regularly in the field, doing such things would set up the exact conditions to potentially drive this into existence.