Studies have shown that neutrophils taken from severe COVID-19 patients are immunosuppressed, with a lack of ability to phagocytose and kill bacteria https://doi.org/10.21203/rs.3.rs-142927/v1 , https://doi.org/10.1101/2020.12.01.406306

It is unclear at this stage whether this defect is programmed into the cells (inherent) or whether it is a result of the in-situ environment – i.e. already activated cells are likely to have a refractory loss of function. This activation has been heavily reported and shown again here with neutrophil elastase deposition in the blood of severe COVID-19 patients, which can predict organ damage https://doi.org/10.1111/all.14746

However, what is clear is that these cells are not as functional against new threats and this may explain the reported secondary bacterial infections in COVID-19. (Note: this will be covered in a future update)