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10.3390/v14010011

http://scihub22266oqcxt.onion/10.3390/v14010011
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35062215!8778683!35062215
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suck abstract from ncbi


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pmid35062215      Viruses 2021 ; 14 (1): ä
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  • Modeling SARS-CoV-2 Infection in Mice Using Lentiviral hACE2 Vectors Infers Two Modes of Immune Responses to SARS-CoV-2 Infection #MMPMID35062215
  • Katzman C; Israely T; Melamed S; Politi B; Sittner A; Yahalom-Ronen Y; Weiss S; Abu Rass R; Zamostiano R; Bacharach E; Ehrlich M; Paran N; Nissim L
  • Viruses 2021[Dec]; 14 (1): ä PMID35062215show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a severe global pandemic. Mice models are essential to investigate infection pathology, antiviral drugs, and vaccine development. However, wild-type mice lack the human angiotensin-converting enzyme 2 (hACE2) that mediates SARS-CoV-2 entry into human cells and consequently are not susceptible to SARS-CoV-2 infection. hACE2 transgenic mice could provide an efficient COVID-19 model, but are not always readily available, and practically restricted to specific strains. Therefore, there is a dearth of additional mouse models for SARS-CoV-2 infection. We applied lentiviral vectors to generate hACE2 expression in interferon receptor knock-out (IFNAR1(-/-)) mice. Lenti-hACE2 transduction supported SARS-CoV-2 replication in vivo, simulating mild acute lung disease. Gene expression analysis revealed two modes of immune responses to SARS-CoV-2 infection: one in response to the exposure of mouse lungs to SARS-CoV-2 particles in the absence of productive viral replication, and the second in response to productive SARS-CoV-2 infection. Our results infer that immune response to immunogenic elements on incoming virus or in productively infected cells stimulate diverse immune effectors, even in absence of type I IFN signaling. Our findings should contribute to a better understanding of the immune response triggered by SARS-CoV-2 and to further elucidate COVID-19.
  • |*Disease Models, Animal[MESH]
  • |Angiotensin-Converting Enzyme 2/*genetics/metabolism[MESH]
  • |Animals[MESH]
  • |COVID-19/*immunology/virology[MESH]
  • |Cell Line[MESH]
  • |Humans[MESH]
  • |Immunity/genetics[MESH]
  • |Lentivirus/*genetics[MESH]
  • |Lung/immunology/virology[MESH]
  • |Mice[MESH]
  • |Mice, Transgenic[MESH]
  • |Receptor, Interferon alpha-beta/genetics[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Transduction, Genetic[MESH]


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