Assume that (during the first week of Covid) the lymphoid organ produced two dozens of high affinity B-cell-antibodies for the same number of epitopes on the viral proteins (after numerous rounds of antigen presentation, hypersomatic mutation, affinity maturation). They circulate into the bloodstream and reach the place causing the inflammation : the lung.

Is there a second round of selection inside the infected lung in term of how much viral proteins, viruses and infected cells the antibodies succeed to bind, provoke opsonisation, apoptosis, phagocytosis ?

One year later if you encounter the same virus again, you'll have only a low level of circulating B-cells-Ab and only those binding to the "true" antigens will multiply, very fast, directly into the infected lung. This third round of selection probably happens already during the second round and I wonder how close to a true efficiency selection it can be. I know that B-cell-receptor-bound-to-antigen endocytosis followed by expression on the cell surface and interaction with T-cells is the main pathway for B-cell activation and multiplication, but it is hard to guess how it interacts with the concept of true efficiency selection. Also since most vaccines can't mimick such a round of true efficiency selection it would explain why some of them fail to be protective (antibody-dependent enhancement..).

Not that anti SARS-CoV-2 N antibody has by far the highest level whereas it is not likely to be very effective against virions and infected cells (since N is hiding inside)


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