Cell death and inflammatory response are the two essential components of our innate immunity response. A recent study advocated that COVID-19 patients overreact to the virus that may be deleterious to the host.

The current COVID-19 pandemic has put everyone at risk. The virus is powerful enough to kill in some people while in others it is relatively mild. This depicts that the range of innate immune responses is unpredictable and diverse.

Utilizing a set of sensors, macrophages identify the pathogen and produce cytokines. They also order the adaptive immune system to recognize the pathogen and ultimately produce antibodies. This provokes inflammation and recruits other innate immune system cells for help.

In order to endure within the living host, pathogens try to silence the inflammatory response. They actually hamper the macrophages' ability to release cytokines and warn the rest of your immune system. To cope up with the virus’s silencing, the infected living cells commit suicide/cell death. Cell death is valuable at the level of the organism (although harmful at the cellular level) because it aids termination of pathogen's proliferation.

Cytokines like TNF (tumor necrosis factor), IL (interleukin)-6 and 1b, guide neutrophils from the blood vessels to the infected tissue area. These cytokines can enhance your body temperature, elevate heartbeat, trigger blood clots that trap the pathogen, and stimulate the brain neurons to modulate physiological responses that have evolved to kill the pathogen.

During a cytokine storm, vasodilatation leads to low blood pressure and considerable blood vessel injury. The storm stimulates the white blood cells to enter the lungs. This invites more immune cells to kill virus-infected cells subsequently leading to organ failure.

In COVID-19 pathology, the cytokine storm leads to destructive consequences for the host. When the cells cannot end the inflammatory response, the cytokines production makes macrophages more hyperactive. These cells now destroy the stem cells in the bone marrow causing anemia. Heightened IL-1b may lead to fever and organ failure. Excessive TNF causes extensive death and clotting of cells lining blood vessels. At some point, the storm becomes irreversible and unstoppable.

Breaking the vicious cycle of the cytokine storm may prove to be a valuable strategy for COVID-19 treatments. This can be accomplished by utilizing antibodies to impede the major mediators of the storm, such as IL6, or its receptor that is present on all the human body cells.

TNF inhibition can be accomplished with FDA-approved antibody drugs like Humira or Remicade or with a soluble receptor such as Enbrel that binds to TNF and prevents it from triggering the inflammatory response. Currently, the global market for TNF inhibitors is US$22 billion. Thus, clinical trials are ongoing to test whether drugs that block various cytokines are effective for stopping the deadly spiral in COVID-19.