Additionally, Major et al. (151) described the role of types I and III of IFN in lung repair during viral infection. The production of IFN-α/β and IFN-λ in C57BL/6 mice was detected immediately at the early stage of influenza virus infection and decreased over time, having reached undetectable levels at the onset of epithelial recovery. Interestingly, the treatment with IFN-α, β, or λ during the recovery phase reduced the proliferation type II alveolar epithelial cells by activation of IFN-induced p53, aggravating lung injury, disease severity, and susceptibility to coinfections. Therefore, time and duration of IFN are critical factors for viral infection response and should be thoroughly considered as a COVID-19 therapeutic strategy.