Our hypotheses were that suppression of viral entry into the cell could be achieved through inhibition of ACE2 and TMPRSS2 expression, that blocking viral infection will reduce the spread of SARS-CoV-2 and allow the innate immune system and antivirals such as remdesivir to more effectively suppress viral infection, and that combinations of drugs that reduce ACE2 and TMPRSS2 may be helpful in addressing unexpected effects of remdesivir on ACE2 expression or hydroxychloroquine on active TMPRSS2. This evidence concerns the gene ACE2 and viral infectious disease.