This is informative; an excerpt:

Our immune system consists of two different layers. The first layer is the innate immune system, which acts within minutes of infection to provide kind of a rapid response. This doesn't require any specificity; it is engaged after any kind of infection. But this innate activation is important to triggering the second layer of the immune system, which is the adaptive immune system. In the adaptive immune system, the key players are B cells and T cells; they eventually acquire specificity and memory, which are the basis of the vaccinations. Having those T- and B lymphocytes that are specific to a particular pathogen and provide a memory response in the long term is very important….

If you follow COVID-infected patients over time, their antibody levels do seem to wane to some degree within 2-3 months. But that is not a cause for alarm because that's what happens when you get infected or when you become immunized for the first time. The antibody levels peak within the first couple of weeks and then eventually come down over a few months. That's okay because you still have memory B cells specific to that antigen as well as a T-cell immune response to the viral antigen. So the second time you're exposed to the same virus, you can mount a rapid, specific, and robust immune response. It's likely that you won't feel anything the second time you're infected. It will be a pretty mild or asymptomatic infection….

Long[-lasting] COVID is quite mysterious in terms of what's driving such long-term disease. Also, the symptoms in these patients appear to shift during the course of post-exposure to COVID. I have three hypotheses to explain it, but it could also be a combination of these. The first hypothesis is that a reservoir of virus is hiding somewhere that's activating and reactivating periodically to cause these types of responses. The nasopharyngeal swabs that we currently use to test for the virus are unable to pick up those kinds of reservoirs.

The second hypothesis is related to this. Perhaps it is not reservoirs of infectious virus but bits and pieces of viral RNA or protein that are being retained somewhere in the body that are activating an immune response against the virus and causing these shifting and prolonged symptoms. The third hypothesis is that the infection generates an autoimmune disease. Perhaps the virus is mimicking self-antigens or virus infection, being so inflammatory in this case, and is eliciting autoreactive T and B cells. We are trying to understand which of these possibilities is true. But perhaps all of these things are happening at the same time.

(Thanks to Dr. David Ozonoff for the pointer.)