Figure 1: Proposed Pathogenesis of SARS-Cov-2 Causing Acute Respiratory Distress. This is an image of an acute inflammatory response in the lung alveolus. The inflammatory response to SARS-CoV-2 leads to denuding of the basement membrane and disruption of epithelial barriers leading to accumulation of fluid in the alveoli. Alveolar macrophages are denoted above and release proinflammatory cytokines increasing neutrophil and monocyte infiltration. Alveolar macrophages release IL-6, TNF, IL-8 and other mediators contributing to an inflammatory cascade and cytokine storm. Neutrophils release reactive oxygen species (ROS), matrix metalloproteinases (MMPs), Leukotriene B4 (LTB4), neutrophil extracellular trap (NET) and other mediators. Tissue necrosis factor (TNF) increases an expression of tissue factor that contributes to platelet aggregation. Platelet aggregation leads to microthrombi and thrombi formation. Increased endothelial injury and increases coagulability and along with platelet aggregation lead to a hyper-thrombotic state. AECI (type I alveolar epithelial cell) and AECII (type II alveolar epithelial cell).