The article is based on this study: https://www.sciencedirect.com/science/article/pii/S2589909020300186?via%3Dihub Somebody downloaded sequences of viral RNA from an open source database and compared the proteins created by the sequences with proteins in the human body. He has the theory that if the immune system creates antibodies against these proteins, the antibodies will help the virus after infection. The mechanism is called ADE, antibody-dependent enhancement. Here is a study about SARS-CoV-2 and ADE: https://www.nature.com/articles/s41586-020-2538-8 > At present, there is no evidence that ADE of disease is a factor in the severity of COVID-19. [..] Further, if instances of ADE of disease occur at all, the experience with dengue suggests that this or other types of immune enhancement will be rare and will occur under highly specific conditions. The article describes when ADE happened in the past and how it happened. But it leaves a big question mark: Why isn't ADE a big problem that occurs with every second virus? There must be a mechanism to avoid the creation of poisonous antibodies. ADE seems to be a bigger problem with viruses with a higher mutation rate because a reinfection triggers antibodies that don't bind to the virus no more. SARS-CoV-2 has a very low mutation rate, so this will not be a problem. If ADE would be a problem with SARS-CoV-2, then the vaccines would prevent this: Vaccines produce only antibodies for the spike protein, while an infection with the virus itself produces much more different antibodies for every part of the virus, amplifying the chance that bad antibodies will be created.