boosters and memory cells

[darkoshi]

I'm eligible for the 2nd COVID-19 booster shot, but have debated getting it now versus waiting a month or two. From what I've read, for people without risk factors, there's no urgency in getting it, and there may be benefits to waiting. (In case there's another big surge several months from now, or in case they come out with new boosters/vaccines based on the latest variants.)

In my area, the current case/hospitalization rates are very low, as low as they were in the very early days of the pandemic.

In two articles, I read something like the following, which I was curious about:

How Long Does It Take for the COVID Booster to Be Effective? (2021/12/21)

There's one other factor that can impact the effectiveness of a booster: time between doses. According to Penaloza-MacMaster, the longer the interval between your original vaccine series and the booster dose, the better antibodies your memory cells can create.

Why would the memory cells work better with a longer interval? So I tried to find an answer (I don't believe I did), and more info on these memory cells...


What to know about booster shots and third doses of the COVID-19 vaccine (2021/12/22)

COVID-19 vaccines create high levels of antibodies that can block the virus from ever infecting our cells. As time passes after your vaccination, however, you also develop memory B cells and T cell immunity and antibody levels go down. With fewer blocking antibodies, the virus might be able to start an infection. As viruses evolve, strains that can bypass those antibodies have an advantage and some people have such a high-level exposure that it can overwhelm the antibodies they do have. When this happens, we call it a “breakthrough infection,” but memory B cells and T cells are able to respond quickly and stop the infection before too much damage is done.

Breakthroughs, Boosters, and B cells … Oh My! (2021/10/12)

Over time, as the infection resolves and these antibodies fail to find virus, they will diminish in number. However, what doesn’t go away are the cells that can produce antibodies against the infecting virus. They are called memory B cells. We also have memory T cells that remain after an infection. If we are exposed to the same virus again, those B and T cells will recognize it and become activated.

The memory B cells will change into another type of B cell, called a plasma cell, and quickly start producing large quantities of antibodies. The antibodies produced by these cells are significantly more effective at stopping the virus than antibodies produced during the first encounter with a virus.

Activated memory T cells will cause the production of chemicals critical to our immune response, called cytokines.

This page has a nice simple chart:
Viral Attack: Memory Cells

Toward the end of each battle to stop an infection, some T-cells and B-cells turn into Memory T-cells and Memory B-cells. As you would expect from their names, these cells remember the virus or bacteria they just fought. These cells live in the body for a long time, even after all the viruses from the first infection have been destroyed. They stay in the ready-mode to quickly recognize and attack any returning viruses or bacteria.

Quickly making lots of antibodies can stop an infection in its tracks. The first time your body fights a virus, it can take up to 15 days to make enough antibodies to get rid of it. With the help of Memory B-cells, the second time your body sees that virus, it can do the same in thing 5 days. It also makes 100 times more antibodies than it did the first time. The faster your body makes antibodies, the quicker the virus can be destroyed. With the help of Memory B-cells, you might get rid of it before you even feel sick. This is called gaining immunity.

B cell memory: understanding COVID-19 (2021/02/09)

If the amount of Abs [antibodies] in circulation drops, or if the pathogen varies from the initial infection, the shield may not be protective, and a re-run of the response would be required. This response, triggered by re-exposure to the same or a closely related pathogen, uses the memory B and T cells, incorporating the information acquired in the first response by starting with cells that have already been selected as being strongly reactive. This head start makes memory responses faster, larger, and of higher affinity than the initial response, allowing for rapid negation of the pathogen, often before symptoms develop.
...
Within GCs [germinal centers], B cells rapidly proliferate and, remarkably, deliberately mutate the DNA encoding the epitope-binding component of their antigen-binding receptor, potentially changing its affinity. This occurs as repeated cycles of proliferation, mutation, and selective survival of those B cells with improved binding affinity to antigen. This “selection of the fittest” continues for the duration of the response or until antigen receptor binding strength reaches a maximum, meaning that B cell affinity is improving as the response progresses.

Why are T cells called T cells
T cells (thymus cells) and B cells (bone marrow- or bursa-derived cells) are the major cellular components of the adaptive immune response.

I wasn't even familiar with this organ of the human body:
Thymus
The thymus is located in the upper front part of the chest, ... behind the sternum, and in front of the heart. It is made up of two lobes


Update, 2022/05/29:
Here's another article that mentions memory B and T cells benefitting from delaying the booster, if you've recently had a COVID infection:

Is a second COVID-19 booster right for me?

“An infection acts as a kind of ‘immune boost,’” Ferullo explains, “Getting a booster shot too soon thereafter runs the risk of interrupting and restarting an immune-building process that the infection began,” he explains. “The longer those memory B and T cells have to mature, the better equipped they will be to fight a new infection, so it makes sense to delay a booster for a few months after recovery.”