The A129 (Ifnar1 KO) mice on a 129 background are a type I (α/β) interferon receptor (Ifnar1) gene knockout model. The absence of the IFNAR1 protein in these mice leads to a lack of type I IFN receptor function, thereby reducing immune response and increasing susceptibility to viral infections. Homozygous A129 (Ifnar1 KO) mice are viable and fertile, but they show increased susceptibility to arbovirus infections.

The IFNAR1 gene encodes a key component of the type I IFN receptor, while the IFNGR1 gene encodes the ligand-binding chain (α) of the type II (γ) IFN receptor. AG129 mice, which are knockout models for both the type I (α/β) IFN receptor (Ifnar1) and the type II (γ) IFN receptor (Ifngr1), lack functional IFNAR1 and IFNGR1 proteins, resulting in deficiencies in α/β/γ interferon receptor signaling and heightened susceptibility to viral infections. Homozygous AG129 mice are viable and fertile, and exhibit increased sensitivity to arboviral infections, generating viremia similar to that seen in humans. Compared to IFNα/β/γR KO mice on the C57BL/6 background, the 129-background AG129 mice exhibit more pronounced neurological symptoms after infection.

This strain is a mouse Ace2 gene knockout model that uses gene editing technology to knock out the homologous gene of human ACE2 in mice. The knockout of the Ace2 gene will result in the absence of ACE2 protein expression, and this model can be used for the study of COVID-19. The homozygous Ace2-KO mice are viable and fertile.

The B6-hDPP4 (line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence encoding aa.29~aa.760 of the mouse Dpp4 gene with the human DPP4 gene CDS sequence (aa.29-766), and the BALB/c-hDPP4 (line 2) mouse (Catalog ID: I001189), constructed on the BALB/cAnCya background strain. These models meet the experimental needs of different strain backgrounds.

The B6-hDPP4 (line 1) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Additionally, Cyagen Biosciences has developed B6-hDPP4(line 2) mice (Catalog ID: I001188) on the C57BL/6JCya background strain and BALB/c-hDPP4 (line 2) mice (Catalog ID: I001189) on the BALB/cAnCya background strain. These two models replace the mouse Dpp4 gene p.S29 to part of intron 2 with the Human DPP4 CDS (aa.29-766)-rBG pA expression cassette, meeting the experimental needs for different strain backgrounds.

The BALB/c-hDPP4 (line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence encoding aa.29~aa.760 of the mouse Dpp4 gene with the human DPP4 gene CDS sequence (aa.29-766), and the B6-hDPP4 (line 2) mouse (Catalog ID: I001188), constructed on the C57BL/6JCya background strain. These models meet the experimental needs of different strain backgrounds.

The G129 (Ifngr1 KO) mice on a 129 background are a type II (γ) interferon receptor (Ifngr1) gene knockout model. The absence of the IFNGR1 protein in these mice results in defective gamma interferon receptor function, which reduces natural resistance and may increase susceptibility to certain viral infections. Homozygous G129 (Ifngr1 KO) mice are viable and fertile.

K18-hACE2 mice can be infected with the SARS-CoV-2 virus, resulting in severe disease characterized by weight loss, rapid respiration, hunched posture, and immobility. This strain responds to viral attack in a dose-dependent manner, thus allowing the study of severe acute respiratory disease in mice heavily infected by high doses of the virus, as well as the long-term effects of low doses of mild infection. The model should be handled in strict accordance with the guidelines for the prevention of SARS-CoV-2 virus infection in humans as specified by CDC&ABSA&WHO, and appropriate personal protective equipment (PPE) and handling methods should always be used when using these mice for research.

This strain is a human ACE2 (hACE2) conditional overexpression model generated by integrating the hACE2 gene expression element into the mouse ROSA26 safe harbor site. Under normal conditions, the expression of hACE2 is blocked by the upstream loxP-Stop-loxP expression stop cassette. Upon mating with Cre mice, the Cre recombinase mediates the deletion of the sequence between the loxP sites, including the stop cassette, thereby enabling the expression of hACE2. When bred with tissue-specific Cre mice, overexpression of the hACE2 gene and protein can be achieved in specific tissues of the offspring mice. Homozygous ROSA26-LSL-hACE2 mice are viable and fertile.

This strain is a mouse Ace2 gene humanization model that uses gene editing technology to replace the endogenous mouse Ace2 gene sequence with human ACE2 CDS, preserving the mouse signal peptide sequence and achieving hACE2 expression directed by the endogenous mouse Ace2 regulatory element. This gene is located on the mouse chromosome X and homozygous females and heterozygous males are viable and fertile.