Thomas is right, the immune system, including B cells that are best know for making antibodies but that also have other functions such as antigen presentation and cytokine secretion, keeps the residual HBV in check in the vast majority of folks who do not suffer immunosuppression, such as from HIV co-infection or organ transplant.
A bit more detail: Basically, we know that this reservoir of cccDNA exists in the body and some of the triggers that cause it to resurge. However, we know next to nothing beyond those 2 points for sure. We don’t even know for sure the reservoir is in the liver, although that is by far the most likely spot.
Persistence of the cccDNA actually explains a confusing thing about HBV immunity after an acute infection: Robust immune responses, including lots of anti-HBs antibodies in the blood, last for many decades after viral clearance without the “antigen re-stimulation” that is often needed to keep memory immune responses from gradually waning. This has led to the hypothesis that the residual low level of cccDNA induces HBV replication at extremely low levels (perhaps intermittently), and this replication is promptly squashed by the immune system. In this scenario, the HBV proteins made during the brief reactivations would restimulate the immune system and keep it robust. This is an unproven hypothesis, but is quite plausible and I suspect it is correct.
To specifically answer your questions:
- Reactivation is extraordinarily unlikely if you are anti-HBs positive.
- The T-cells probably do kill the infected cells, but T cells are hampered in the liver because it is an “immuno-privileged site” that dampens immune responses. The reason for that is because the antigens in the food we eat go through the liver first, and everyone would die of food allergies if the liver was not an immunosuppressive environment. That means the immune system essentially has to fight HBV with one hand tied behind its back.
- We do not know if the residual HBV is completely dormant or just turned way down. We won’t be able to figure that out till we find where the cccDNA is hiding in the body. The studies that have been done can’t find any residual antigen in the liver, but the assays that need to be used in those studies (mostly immunohistochemistry) are not very sensitive and easily could miss very low levels of HBV proteins.
- We suspect the residual HBV is constantly trying to replicate but the immune system is constantly suppressing it. If that is true, HBV senses immunosuppression by the absence of pressure against it.
- Total killing of cccDNA-containing cells is what would be expected, but does not happen. Again we don’t know for sure why, but the immuosuppressive nature of the liver is likely to be one cause (but unlikely to be the only one).
I hope this helps.