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Mnementh said:
sethnintendo said:

a) B- and T-cells *are* you're learned immune answer. Both cell-types react to specific proteins or other molecules. In a case of an infection the body tries to identify proteins specific to the attacker (either virus or bacteria) and reproduce B- and T-cells with receptors for that molecule. After an infection both types of cells have some variants that live longer, these are memmory cells. The memory cells can in case of a new infection with the same virus or bacteria be reproduced very quickly. B-cells produce antibodies, that connect to the molecule they identify and destroy it. T-cells kill cells that show the molecule that they identify, in case of a viral infection they kill the cells of your own body that are infected and reproduce more of the virus.

b) Scientist don't know a lot about many things. Still, they also know a lot already and this current knowledge has already applications. For how long an achieved immunity will hold: too many factors are unclear yet. That doesn't mean we can expect a long-lasting immunity.

c) Maybe. You just said scientists don't know everything. There are different projections on how many people got already infected. You chose one on the higher end. So, what scientists really say is: *up* to 20 million may have been already infected. But maybe less.

d) As I answered in a, our immune response reacts to certain molecules. If a mutation changes these molecules, so that the receptors don't work anymore, you still need a new immune respone. Your immune system may react to multiple molecules from the infection. In that case changing one molecule will lead to partial immunity, as other receptors still work. Also some receptors may check for molecules, that are needed for the functioning of the virus, so that any change in that renders the virus harmless. But it is all a maybe, maybe your immune system only picks one specific molecule, maybe that can mutate and the virus will still work.

While what you said in the other points is mostly right on a simplified fashion (although the CDC estimate lies on the lower end and a recent study argues infections in the US might be underreported 27 times), each pathogen will have a certain number of accessible antigens, and each antigen will have a number of epitopes (that is to say, parts of it to which an antibody can bind) and each of the trillion B or T cells in your organism will also have different expressivities of assembling mechanisms based on genetic factors, cytokine signaling etc.
Of course, out of these there will ultimately be convergence selected by experience on what is able to effectively protect you. But even then we are talking about a fair number of them (on average 10 - 20 for each antigen) enduring in the immune system repertoire that will balloon to the millions with somatic mutations, each with their own affinity and specificity. So to expect that immunity could depend on a single thread that might break at any moment at the whims of pathogen mutation and cellular death is as naïve as believing you can forget your mother exists if one of your neurons randomly dies.
That being said, someone, somewhere, will probably be unlucky enough to have such a crap immune response that they will be able to be reinfected in a month, while a few people, a bit like the MERS study I've cited earlier, that will not only be immune to it for life, but also won't contract any coronavirus strain ever again.