Despite virus induced activation of immune cells, overproduction of pro-inflammatory cytokines and chemokines (TNFα, IL-6, IL-8, CXCLs), and the possible development of acute respiratory distress syndrome (ARDS), a key feature of the infection is low production of type I and type III IFNs in the early stages of illness [26,27]. This evidence concerns the gene TNF and acute respiratory distress syndrome.