@VincentRK @manal_mehta @jhuber 1/n Important discussion with several unresolved questions. First, there are people with T cells to SARS-Cov2 because they have been exposed to other beta-coronaviruses. There is substantial homology in the nucleoproteins. This is shown in 2 papers, including the Nature paper.
@VincentRK @manal_mehta @jhuber 2/n Are these people "immune" to SARS-Cov2 or do they get attenuated disease ? We don't know. Do they spread virus ? We don't know. Intriguingly, the number is around 40% which is around the number that were not infected in the Antarctic cruise.
@VincentRK @manal_mehta @jhuber 3/n Second: we know that the antibody titer AFTER infection has attrition over time, especially if infection is not severe. How do we define "seroprevalence" ? At what cutoff -- since it's a moving target for some people ?
@VincentRK @manal_mehta @jhuber 4/n Let's say we cutoff at 1.4 (arbitrary units). What if you have 1.1 ? Are you immune ? We have no idea ? What if you are 0.3 after 6 months ? Can you get re-infected, or will you have an attenuated disease ?
@VincentRK @manal_mehta @jhuber 5/n And we aren't even measuring the T cell response and B MEMORY response when we measure an antibody titer. So do these predict the limits of infection? If you have a low Ab titer, but B mem and T cells, are you immune?
@VincentRK @manal_mehta @jhuber 6/n Try explaining this to people who have no background in virology, immunology or T cell biology. The point is that we are extremely "unversed" in viral PATHOLOGY
