DIAGRAM EXPLANATION

Excessive inflammatory responses are a function of

(1) viral exposure or inoculum,
(2) the presence/absence of comorbidities, and
(3) the state of immunocompetence, and are characterized by excessive
release of inflammatory cytokines such as interleukins 1, 6, 8, 17,:
-interleukin1 1β(cytokine interleukin-1β (IL-1β) is a key mediator of the inflammatory
response)
- interleukin 6, is responsible for stimulating acute phase protein
synthesis, as well as the production of neutrophils in the bone marrow.
It supports the growth of B cells and is antagonistic to regulatory T
cells.
- inteleuken 8, attracts and activates neutrophils in inflammatory
regions.
- interleukin 17,  that acts as an inflammation mediator.

monocyte chemoattractant protein-1 ( one of the important chemokines that

controls migration and infiltration of monocytes/macrophages during
inflammation),and tissue necrosis factor α [11] alpha fetoprotein( protein
produced primarily by the liver) collectively known as “cytokine storm”

(4) this process results in the development of acute lung injury (ALI), acute
respiratory distress syndrome (ARDS), coagulopathy, hypotension, hypoperfusion,
organ failure (also known as multiple-organ failure (MOF) or multiple-organ
dysfunction syndrome (MODS)), and death, as shown in our diagram.
* post-septic patients are prone to latent virus reactivation
COVID-19 patients are at risk for the development of secondary bacterial and fungal
infections , highlighting the immune suppression and dysregulation.