So, you need to take two big jumps from concrete data to get to that point. One big jump is assuming the people infected with the endemic coronaviruses will generate these CD4 cells that recognize SARS-COV2. What if it's due to a completely unrelated antigenic protein that is similar, or if it is from an endemic coronavirus, are all equally effective at inducing these cells or is it only some.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.
And then the second jump you need to make is whether the presence of these cells is at all clinically relevant. Perhaps humoral immunity (antibody mediated) is more important, and even a competent cellular immune response is not sufficiently protective.
Now that other preprint article goes some ways to answering the first question I posed. They showed 34% of serology negative patients had CD4 cells that could recognize SARS-COV2 peptides, but they recognized only portions of the spike protein that were most similar to the portions conserved in other endemic coronaviruses, as opposed to the CD4 cells of covid+ patients, which recognize several different areas of the SARS-COV2 spike protein.
These two papers do have me feeling good though. I think with some defensible assumptions, infection in the past few years with an endemic coronavirus may give some degree of immunity. Those folks may still be at risk of forward transmission. And probably there are patients in whom prior endemic coronavirus exposure does not confer any immunity, probably due to some intrinsic quality of their immune system. In the preprint paper they found 100% of tested samples had antibodies to endemic coronavirus, but not all of them had helper T cells that recognized the SARS-COV2 peptides. I couldn't find the supplemental figure for this though.
And yeah, a cohort study would need to be big and long term, unless you could do it in a hot spot area. I imagine there is some good cell culture and animal research that could fill in gaps and be done in a relatively quick timeframe as well.