Physiological modeling and biomechanical insights of cytokine modulation in COVID-19 and pulmonary fibrosis through graph-based approach

Coronavirus disease (COVID-19), due to its high virulence, has infected millions worldwide, causing a lot of deaths among infected patients. The SARS-CoV-2 virus, which primarily affects the respiratory system and the cardiovascular tissues during its progression, was the primary cause of the illness. Cytokine Release Syndrome (CRS) is one of the leading reasons for the tissue damage that occurs during the viral infection in COVID-19. CRS is accompanied by the abnormal release of cytokines and immune cells, which is due to the faulty regulation of genes and target proteins, which are further responsible for the overall functioning of cytokine activity within the immune system. When the modulation of cytokine activity gets disturbed due to alterations in the biological pathways associated with the healthy functioning of immune proteins, abnormal concentrations of inflammatory proteins are deployed to the site of infections where excessive inflammatory responses occur, which again leads to the destruction of cells and tissues they are exposed to. A similar process occurs in the pulmonary tissues, where viral pathogenesis in patients with a history of pulmonary conditions leads to the development of CRS. This condition damages the tissues that make up the structure of the lungs. Abnormal expression of fibrotic proteins and uncontrolled release of cytokines then lead to the formation of fibrosis structures in the lung tissues. This progression can result in a medical emergency due to the risk of inflammation within the lung network and respiratory failure. In this study, we established different graph-based modeling approaches to elucidate a mechanistic understanding of cytokine modulation and its association with COVID-19 and pulmonary fibrosis. ![Figure][1] ### Competing Interest Statement The authors have declared no competing interest. [1]: pending:yes