"Frozen lung tissue was stained for SARS-CoV-2 N protein (red) and epithelial cells (EpCAM, green)."

Johns Hopkins University

Currently, human entry receptor angiotensin-converting enzyme 2 (hACE2) transgenic mice are being used to study SARS-CoV-2 infection and pathogenesis, but these transgenic mice are limited to only one genetic background and are not widely available.  Thus, another mouse model of SARS-CoV-2 using adeno-associated virus (AAV)-mediated expression of hACE2 has been developed.  These AAV-hACE2 mice are capable of allowing for viral replication and demonstrate the pathogenicity of the virus as seen in patients with COVID-19.  

AAV-hACE2 Mouse Model of SARS-CoV-2

Benjamin Israelow, Eric Song, Tianyang Mao, Peiwen Lu, Amit Meir, Feimei Liu, Mia Madel Alfajaro, Jin Wei, Huiping Dong, Robert J. Homer, Aaron Ring, Craig B. Wilen, Akiko Iwasaki; Mouse model of SARS-CoV-2 reveals inflammatory role of type I interferon signaling. J Exp Med 7 December 2020; 217 (12): e20201241. doi: https://doi.org/10.1084/jem.20201241

Mouse model of SARS-CoV-2 reveals inflammatory role of type I interferon signaling

Figure of Frozen Lung Tissue from AAV-hACE2 Mice Infected with SARS-CoV-2

Researchers have demonstrated using AAV-hACE2 mice that type I interferons play a key role in inducing pathological responses, but do not regulate the replication of SARS-CoV-2 in vivo.  Specifically, to recruit and activate proinflammatory cells to the lungs upon infection with SARS-CoV-2, type I interferon signaling is necessary.  However, type I interferon signaling is not enough for the clearance of the SARS-CoV-2 infection, as indicated by the absence of viral clearance in AAV-hACE2 mice that lacked type I interferon signaling. 
  

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