ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) shows high binding affinity toward hACE2 receptors, which are present across the body, and thus this interaction can involve multiple organs of the body during the infection. Due to varied level of host response, type of strain, host condition (comorbidity), and viral load, COVID-19 can be mild, moderate, or severe. Advancement or severity of disease can lead to the cytokine storm, resulting in hyper-inflammatory stage or sepsis storm, which can end in death. Multiple-organ involvement among various patients in a sequential course is not linked to load of virus. Complications like inflammation, thrombophilia, endothelial dysfunction, vasoconstriction, platelet activation, stasis, low blood oxygen, and immobilization of muscles are commonly found in severe hospitalized cases. Lungs are the prime target of SARS-CoV-2, which causes pulmonary fibrosis and acute respiratory distress syndrome (ARDS). In severe cases, cardiovascular-associated complications such as myocarditis can be present. Renal- and hepatic-associated complications have also been reported, which are generally secondary to systemic derangements. Central nervous system (CNS) involvement that can result in complications like inflammation of the meninges, acute inflammation of the brain, stroke, and disturbance in mental abilities has also been observed. Psychological imbalances are also common. Gastrointestinal tract (GIT) complications can result in diarrhea. Impairment in sense of odor and flavor is observed. Furthermore, organ failure can be caused by the cytokine storm, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs. Thus, it is important to identify the exact mechanisms of pathogenesis in order to improve the outcomes and decrease the rate of mortality and morbidity.
