Antibodies are supposed to be the good guys. The proteins, built of distinctive Y-shaped pieces, enter the bloodstream early in infection, pouring out from plasma cells. They then latch onto molecules festooning pathogens and alert natural killer cells, which release a torrent of cytokines and complement, which are the biochemical weapons of an immune response.
Fighting infection is a complex business.
In a mysterious phenomenon called "antibody-dependent enhancement," the proteins actually make matters worse, intensifying symptoms. When a vaccine elicits the errant antibodies, the backfiring is called "vaccine enhancement of disease." We know these reactions exist, but still do not completely understand them.
The turncoat antibodies can be coaxed to appear in test tube experiments, but are elusive in a patient who is getting sicker. That is, there's no clinical way to distinguish antibody-dependent enhancement from just a severe case of an infectious disease. And that can complicate analysis of a candidate vaccine. "Vaccine enhancement of disease" would show up in a clinical trial as more people receiving a vaccine getting sick than the participants getting placebo.
Reportedly that hasn't happened for the candidate COVID-19 vaccines, but the data won't be published until the phase 3 trials are completed.
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