By the way, here is an explanation of how covid killed by triggering the cytokine storm, autoimmune response.
Which means our own immune system causes covid deaths.
{...
Accumulating evidence suggests that the severity of COVID-19 is associated with an increased level of inflammatory mediators including cytokines and chemokines such as interleukin (IL)-2, IL-7, IL-10, tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), monocyte chemoattractant protein-1 (MCP1; also known as CCL2), macrophage inflammatory protein 1 alpha (MIP1α; also known as CCL3), CXC-chemokine ligand 10 (CXCL10), C-reactive protein, ferritin, and D-dimers in blood upon SARS-CoV-2 infection [2–10]. Of note, among the elevated inflammatory mediators, the blood IL-6 level is highly correlated with the disease mortality when COVID-19 survivors and non-survivors are compared [1, 11], suggesting that fatal COVID-19 is characterized as a cytokine release syndrome (CRS) that is induced by a cytokine storm with high mortality [12–14]. Thus, IL-6 serves as a possible mechanism of treatment for severe COVID-19 patients, raising the possibility that one therapeutic option for the disease may be targeting excessive inflammation caused by IL-6 receptor (IL-6R) signaling with monoclonal antibody therapy or treatment with chemical modulators to block the signaling cascade while maintaining a sufficient antiviral primary immune response. In this regard, the use of two clinically approved IL-6R antagonists, tocilizumab (TCZ) and sarilumab (SAR), which are currently used for the treatment of rheumatoid arthritis, could be expected to play a crucial part in the treatment for severely ill patients. With this in mind, here we discuss the potential pathogenetic mechanisms and therapeutic options for COVID-19, focusing on IL-6-signal transducer and activator of transcription 3 (STAT3) signaling.
...}
Cytokines, chemokines, and phages are antibodies produced by the immune system.