| There is no reason to believe that SARS-CoV-2 attacks the immune system. The study that suggested ADE for this virus showed a very mild effect in vitro. However, antibodies still prevented infection. More crucially yet, a high number of viruses exhibit ADE in vitro, yet only two exhibit ADE in vivo. Moreover, even in vitro, infection of immune cells by the virus did not lead to viral replication. It's therefore unlikely that it shows ADE in humans, especially since its far less severe than viruses that do. You might notice that for critical cases, lymphocytes counts are down. The issue is that lymphocyte counts are low, yet those patients show very high cytokine levels, and lymphocytes also exhibit exhaustion. Studies in a clinical setting have shown that indeed cytokine levels are a good predictor of lower lymphocyte counts. Thus this seems better explained by the cytokine storm. Another thing that's good to know is that this coronavirus seems to have a very good exoribonuclease, which is an error checking enzyme. Mutation rates are also quite low, empirically. It is thus probable that this virus will not evolve too much. Finally, the study that suggests that there are two lineages is deeply flawed. When you take into account the founder effect of international dissemination right before border controls are implemented, and the low mutation rate, you will find that the observation that led to the conclusions that there are two strains is not significantly more likely than the null hypothesis that this is simply a coincidence. Therefore it is not possible to make conclusions about the existence of strains, and certainly not possible to suggest they would behave differently in any way. |
(One of which was that biologists have a more specific definition of "virus attacks X system" than computer security researchers, so my wording seems to have been off there. I was trying to say "seems to do something against its effectiveness, because we see cases of reinfection after a short time")