There are several limitations to these two options. Regarding the SARS RBD strategy, the body would likely develop an immune response to the SARS protein eventually, although the key intervention period of infection to combat 2019-nCoV would fall under this window of time, where after an immune response for both viruses would develop. Alternatively, if one were to use the homologous RBD from 2019-nCoV itself, this immune response would likely be very advantageous since it could yield both a blocking effect and a vaccination effect 52. For both strategies, the dose that would be needed to block ACE2 receptors in the body across different organs is unknown, and as is the percentage of ACE2 receptors that would need to be saturated in order to slow the infection. The number of ACE2 receptors in the body, which are found in lung and gastrointestinal organs along with vascular endothelial cells among other tissues 53, could ultimately prove prohibitive for this strategy. Moreover, the turnover of the ACE2 receptor on the cell surface would also influence how often the therapeutic protein would need to be administered. To solve this issue, one could increase the concentration of anti-ACE2 therapy at the crucial site of infection in the lungs, via local administration to lungs via nebulization. Lastly, there is the possibility that binding ACE2 directly could paradoxically worsen lung physiology and clinical symptoms. A study found that a fusion protein of SARS RBD to Fc domain bound ACE2 in murine lung tissue after administration, exacerbating alveolar edema via ACE2 interaction, which normally counteracts acute lung injury 54. This suggests that if one were use an ACE2 binding strategy, it would be best employed early during infection or as a prophylaxis to block the initial viral infection. Ultimately, clinical trials in patients would need to investigate these potential issues.