Great question, @Aman. And thanks @A7xImpulse for a great summary of the most recent research (which we have published on Mitosis of hepatitis B virus-infected cells in vitro results in uninfected daughter cells - ScienceDirect and has been highlighted by a PhD student working in my lab - Example entry: Hepatitis B cccDNA viral reservoirs - stubborn nails in the quest for a complete cure). I am really so glad that we’ve been able to get such sophisticated complex concepts taken up by the community.
Some additional comments:
The average lifespan of a liver cell is about 6 months, which is fairly long when you think about it. This is why the reduction of cccDNA even while on therapy is very slow.
At the start of an infection (immune tolerance phase) pretty much the entire liver is infected. But when you are in HBeAg-negative phases, something like 1% of liver cells are infected (even when there’s plenty of virus around to infect the other cells). We still don’t know the underlying reason for this and if the one that are infected really represent a different type of cell.
Indeed, I’ve been on antivirals for many years and my levels of HBeAg and HBsAg have remained quite high through the years.
Thomas