> Anyone with more experience in immunology care to weigh in on why the second paragraph there follows from the first? Naively, one might expect targeting a wid

> Anyone with more experience in immunology care to weigh in on why the second paragraph there follows from the first? Naively, one might expect targeting a wider variety of places on on the COVID spike protein to result in better immunity against variants, not worse. Why is the article saying the opposite? The RBD is the part of the spike protein that latches onto the cell. Specifically it latches onto the ACE2 receptor. If the RBD changes too much then the virus can no longer infect its target cells (because it can't attach to ACE2 receptors). This means that there are probably strong limits on how much this section of the virus can change. Because we expect the RBD to change less than other areas, and because the mRNA vaccines recognize more of these possible changes, then we have a reasonable expectation that mRNA based immunity should continue to be effective. To make a crude analogy, ACE2 is a phillips head screw. The spike protein is a phillips screw driver. The tip of the screw driver is the RDB. Infection elicited antibodies recognize random spots all over the screw driver. mRNA vaccine elicited antibodies recognized spots all over the tip. Eventually you can turn the handle into a shape that won't be recognized, but there are strict limits on how much you can change the tip while still having it function as a philips screw driver. And of the ways that you can change the tip, the mRNA antibodies will match more of them than the naturally acquired ones. At least that's the expectation. There are still possible ways that the virus might evade; perhaps by making shields for the tip that block portions of the antibody, but this seems like it might be harder than changing the handle's shape.