The disease caused by SARS-CoV-2—CoVID-19—is a globalpandemic that has brought severe changes worldwide. Approximately80% of the infected patients are largely asymptomatic or have mildsymptoms such as fever or cough, while rest of the patients display vary?ing degrees of severity of symptoms, with an average mortality rate of3–4%. Severe symptoms such as pneumonia and acute respiratory dis?tress syndrome may be caused by tissue damage, which is mostly dueto aggravated and unresolved innate and adaptive immune response,often resulting from a cytokine storm. Here, we discuss how an intricateinterplay among infected cells and cells of innate and adaptive immunesystem can lead to such diverse clinicopathological outcomes. Particu?larly, we discuss how the emergent nonlinear dynamics of interactionamong the components of adaptive and immune system componentsand virally infected cells can drive different disease severity. Such mini?malistic yet rigorous mathematical modeling approaches are helpful inexplaining how various co-morbidity risk factors, such as age and obe?sity, can aggravate the severity of CoVID-19 in patients. Furthermore,such approaches can elucidate how a fne-tuned balance of infectedcell killing and resolution of infammation can lead to infection clearance,while disruptions can drive different severe phenotypes. These resultscan help further in a rational selection of drug combinations that caneffectively balance viral clearance and minimize tissue damage.
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