Mouse line | Disease model | Key findings | [Ref.] |
Wildtype | SARS | SARS-CoV infections resulted into shedding of large amounts of infectious virus with the development of lung injury due to lowering of ACE2 expression | [64] |
SARS | SARS-CoV-infected C3−/− mice exhibited significantly less weight loss and less respiratory dysfunction with reduced lung pathology and lower cytokine and chemokine levels in both the lungs and the sera | [65] | |
Ace2−/− | SARS | SARS-CoV infections resulted in less shedding infectious virus with mild lung pathological changes due to reduced amount of spike RNA | [64] |
ARDS/SARS | ACE2 blockade in mice resulted into enhanced vascular permeability, increased lung oedema, neutrophil accumulation, and worsened lung function | [53, 64] | |
Tmprss2−/− | SARS | SARS-CoV infection in Tmprss2−/− mice showed attenuated inflammatory chemokine and/or cytokine responses | [33] |
COVID-19 | Transcriptional downregulation of Tmprss2 inhibits host SARS-CoV-2 entry. | [63] | |
Tmprss2−/− hDPP4-Tg | MERS | Tmprss2−/− murine models infected by MERS-CoV showed improved immunopathology | [33] |
hACE2 | COVID-19 | Mouse model of COVID-19 showing similar pattern of human interstitial pneumonia with infiltration of significant macrophages and lymphocytes into the alveolar interstitium, and accumulation of macrophages in alveolar cavities following SARS-CoV-2 infection | [6, 7, 66] |
hACE2 | COVID-19 | This model developed productive SARS-CoV-2 infection and inflammatory pulmonary infiltrates as seen in COVID-19 patients Evidence of inadequate antiviral activity and potential harms of endogenous type I IFN responses were observed | [5] |
C3−/− | SARS | SARS-CoV-infected C3−/− mice exhibited significantly less weight loss and less respiratory dysfunction with reduced lung pathology and lower cytokine and chemokine levels in both the lungs and the sera | [65] |
Ace2−/−: angiotensinogen converting enzyme 2 knockout; SARS: severe acute respiratory syndrome; CoV: coronavirus; C3−/−: complement 3 knockout; ARDS: acute respiratory distress syndrome; Tmprss2−/−: transmembrane protease, serine 2 knockout; COVID-19: coronavirus disease 2019; hDPP4-Tg: human dipeptidyl peptidase 4 transgene; MERS: Middle East Respiratory Syndrome; hACE-2: transgenic mice bearing human ACE2; IFN: interferon.