By the time a COVID-19 patient presents with dyspnea, the virus has spread through the body, so as with influenza and Tamiflu, an antiviral administered at this point may have modest therapeutic benefit. The morbidity/ mortality is due to a cytokine storm causing innate immune cell infiltration into, and concomitant damage to, the lungs. In a positive feedback loop, the damage causes further cytokine release and further immune cell influx. We are testing potential therapeutics to try to block the positive feedback loop. We have developed a BSL1 mouse model that mimics the monocyte/macrophage increase, the clot-like platelet aggregates, and the relative lack of neutrophils in the bronchoalveolar lavage fluid, and alveolar wall thickening seen in COVID-19 autopsy lungs that differentiate this from ARDS. We will be happy to share the model.