Hamsters Expressing Human Angiotensin-Converting Enzyme 2 Develop Severe Disease following Exposure to SARS-CoV-2
The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While...
Saved in:
| Published in | mBio Vol. 13; no. 1; p. e0290621 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
22.02.2022
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease.
The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2.
IMPORTANCE
The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. |
|---|---|
| AbstractList | The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus.The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. ABSTRACT The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus. |
| Author | Stevens, Stephen Blue, Eugene Li, Rong Mucker, Eric M. Fuentes-Lao, Amadeo J. Moore, Joshua L. Wang, Zhongde Cline, Curtis R. Liu, Yanan Zeng, Xiankun Davis, Neil Kunzler, Madelyn Golden, Joseph W. Twenhafel, Nancy Hooper, Jay W. Spik, Kristin W. Williams, Janice A. Garrison, Aura R. Stewart, Rebekah Larson, Deanna D. |
| Author_xml | – sequence: 1 givenname: Joseph W. surname: Golden fullname: Golden, Joseph W. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 2 givenname: Rong surname: Li fullname: Li, Rong organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 3 givenname: Curtis R. surname: Cline fullname: Cline, Curtis R. organization: Pathology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 4 givenname: Xiankun surname: Zeng fullname: Zeng, Xiankun organization: Pathology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 5 givenname: Eric M. orcidid: 0000-0002-4656-5379 surname: Mucker fullname: Mucker, Eric M. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 6 givenname: Amadeo J. surname: Fuentes-Lao fullname: Fuentes-Lao, Amadeo J. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 7 givenname: Kristin W. surname: Spik fullname: Spik, Kristin W. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 8 givenname: Janice A. surname: Williams fullname: Williams, Janice A. organization: Pathology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 9 givenname: Nancy surname: Twenhafel fullname: Twenhafel, Nancy organization: Pathology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 10 givenname: Neil surname: Davis fullname: Davis, Neil organization: Pathology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 11 givenname: Joshua L. surname: Moore fullname: Moore, Joshua L. organization: Veterinary Medicine Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 12 givenname: Stephen surname: Stevens fullname: Stevens, Stephen organization: Veterinary Medicine Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 13 givenname: Eugene surname: Blue fullname: Blue, Eugene organization: Veterinary Medicine Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 14 givenname: Aura R. surname: Garrison fullname: Garrison, Aura R. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA – sequence: 15 givenname: Deanna D. surname: Larson fullname: Larson, Deanna D. organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 16 givenname: Rebekah surname: Stewart fullname: Stewart, Rebekah organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 17 givenname: Madelyn surname: Kunzler fullname: Kunzler, Madelyn organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 18 givenname: Yanan surname: Liu fullname: Liu, Yanan organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 19 givenname: Zhongde surname: Wang fullname: Wang, Zhongde organization: Department of Animal, Dairy, and Veterinary Sciences, Utah State University, Logan, Utah, USA – sequence: 20 givenname: Jay W. orcidid: 0000-0002-4475-0415 surname: Hooper fullname: Hooper, Jay W. organization: Virology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35073750$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1kc1v1DAQxS1URD_okSvKESGleJwPOxek1XZhK1VCYoGr5STjxavETu1kafnr691tUYvAl7Fmnn96nndKjqyzSMgboBcATHzoa-MuKKtomTJ4QU4YFDTlBcDRk_sxOQ9hQ-PJMhAZfUWOs4LyjBf0hNwsVR9G9CFZ3A4eQzB2nSynXtlkZtfGjWhjK507u0U_7oYL-_uux4Qll7jFzg3JKlaPyaUJqAIm2nWd-7VX3g4uTHE0umQ1-7qKlB8pe01eatUFPH-oZ-T7p8W3-TK9_vL5aj67TlUuxJg2tOJMaU45VYXCumo56HgQVQVliUDrRrCcQVtnAnStMy6qFjQXuWZNWWRn5OrAbZ3ayMGbXvk76ZSR-4bza6nij5oOJW-hFlCXTOVlLnQt4nbyBhgTRVXmwCPr44E1THWPbYN29Kp7Bn0-seanXLutFFzwfG_m3QPAu5sJwyh7ExrsOmXRTUGykrGypJBXUfr-IFWhZ3LjJm_jmiRQuYtc7iKX-8glgyh--9TYH0ePAUdBdhA03oXgUcvGjGo0bufTdP_Fpn-9egT_W38PuHLJpA |
| CitedBy_id | crossref_primary_10_1016_j_ebiom_2023_104677 crossref_primary_10_1002_ame2_12471 crossref_primary_10_1038_s41467_023_42796_0 crossref_primary_10_3390_v14081777 crossref_primary_10_1016_j_isci_2023_107764 crossref_primary_10_1080_15548627_2023_2267958 crossref_primary_10_1016_j_antiviral_2023_105605 crossref_primary_10_1038_s41392_024_01917_x crossref_primary_10_51847_KhjrtFnxNb crossref_primary_10_3390_v14040776 crossref_primary_10_1186_s40035_022_00316_y crossref_primary_10_3389_fmicb_2024_1348405 crossref_primary_10_1038_s44298_025_00092_2 crossref_primary_10_1080_26895293_2025_2468334 crossref_primary_10_3390_v16101625 crossref_primary_10_1038_s41467_024_45495_6 crossref_primary_10_1177_03009858221092015 crossref_primary_10_1016_j_autneu_2022_103057 crossref_primary_10_1016_j_bsheal_2022_05_001 crossref_primary_10_3390_cells11152395 crossref_primary_10_1523_ENEURO_0106_24_2024 crossref_primary_10_1016_j_tins_2022_02_006 crossref_primary_10_1038_s42003_024_06015_w |
| Cites_doi | 10.1371/journal.ppat.1008536 10.1016/j.cytogfr.2020.05.003 10.4037/aacnacc2021302 10.1084/jem.20202135 10.1212/WNL.0000000000010979 10.1212/WNL.0000000000010250 10.1016/S1474-4422(20)30221-0 10.1038/nature02145 10.1093/cid/ciaa325 10.1172/jci.insight.142032 10.1016/j.jinf.2020.03.037 10.1016/S2213-2600(20)30079-5 10.3174/ajnr.A6651 10.1073/pnas.2009799117 10.1186/s40463-020-00423-8 10.1126/science.abb2507 10.1038/s41590-020-0778-2 10.36740/WLek202104144 10.1126/scitranslmed.abf8396 10.1111/ene.14277 10.1016/S0140-6736(20)30211-7 10.1016/j.bbi.2020.12.031 10.1002/cjp2.212 10.1084/jem.20200678 10.1128/JVI.02012-06 10.1016/S2666-5247(20)30004-5 10.1128/jvi.78.7.3572-3577.2004 10.1038/s41586-020-2943-z 10.1099/jgv.0.001599 10.1016/j.cell.2020.02.052 10.1038/s41593-020-00758-5 10.1128/JVI.00127-20 10.3201/eid2606.200516 10.1038/s41586-020-2180-5 10.1038/s41586-020-2012-7 10.1101/2021.07.26.453840 10.1016/j.bbi.2020.06.032 10.1093/gerona/glaa149 10.1016/j.coviro.2015.06.009 10.1128/JVI.01683-20 10.1007/s00401-020-02166-2 10.1007/s00415-021-10474-0 10.1084/jem.20200652 10.1016/S2213-2600(20)30243-5 10.3389/fnana.2020.00037 10.1111/jon.12880 10.1172/jci.insight.139042 10.1038/s41586-020-2179-y |
| ContentType | Journal Article |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1128/mbio.02906-21 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE CrossRef |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ (Directory of Open Access Journals) url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2150-7511 |
| Editor | Mahalingam, Marthandan Batra, Himanshu |
| Editor_xml | – sequence: 1 givenname: Himanshu surname: Batra fullname: Batra, Himanshu – sequence: 2 givenname: Marthandan surname: Mahalingam fullname: Mahalingam, Marthandan |
| ExternalDocumentID | oai_doaj_org_article_7d1b81b62a4648fb80734c1228596417 PMC8787465 02906-21 35073750 10_1128_mbio_02906_21 |
| Genre | Research Support, U.S. Gov't, Non-P.H.S Journal Article Research Support, N.I.H., Extramural |
| GrantInformation_xml | – fundername: NIAID NIH HHS grantid: HHSN272201700041I – fundername: HHS | NIH | National Institute of Allergy and Infectious Diseases grantid: HHSN272201700041I/75N93020F00001/A38 – fundername: DOD | Defense Health Agency (DHA) funderid: https://doi.org/10.13039/100009898 – fundername: ; – fundername: ; grantid: HHSN272201700041I/75N93020F00001/A38 |
| GroupedDBID | --- 0R~ 53G 5VS AAFWJ AAGFI AAUOK AAYXX ADBBV AENEX AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV BTFSW CITATION DIK E3Z EBS FRP GROUPED_DOAJ GX1 H13 HYE HZ~ KQ8 M48 O5R O5S O9- OK1 P2P PGMZT RHI RNS RPM RSF CGR CUY CVF ECM EIF NPM - 0R ADACO BXI HZ M~E RHF 7X8 5PM |
| ID | FETCH-LOGICAL-a488t-c0972af7070a5aeb9d71ffffeea9166e10bc82421db381fbf3789d1f784f2c653 |
| IEDL.DBID | M48 |
| ISSN | 2150-7511 |
| IngestDate | Wed Aug 27 01:29:40 EDT 2025 Thu Aug 21 18:08:32 EDT 2025 Fri Jul 11 10:44:44 EDT 2025 Tue Feb 22 21:30:05 EST 2022 Thu Apr 03 06:59:53 EDT 2025 Tue Jul 01 01:52:51 EDT 2025 Thu Apr 24 22:53:12 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | SARS-CoV-2 olfactory bulb transgenic hamsters nasal cavity K18-hACE2 angiotensin-converting enzyme 2 neuropathology cardiac lesions |
| Language | English |
| License | This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-a488t-c0972af7070a5aeb9d71ffffeea9166e10bc82421db381fbf3789d1f784f2c653 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The authors declare no conflict of interest. |
| ORCID | 0000-0002-4475-0415 0000-0002-4656-5379 |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1128/mbio.02906-21 |
| PMID | 35073750 |
| PQID | 2622660149 |
| PQPubID | 23479 |
| PageCount | 16 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_7d1b81b62a4648fb80734c1228596417 pubmedcentral_primary_oai_pubmedcentral_nih_gov_8787465 proquest_miscellaneous_2622660149 asm2_journals_10_1128_mbio_02906_21 pubmed_primary_35073750 crossref_citationtrail_10_1128_mbio_02906_21 crossref_primary_10_1128_mbio_02906_21 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2022-02-22 |
| PublicationDateYYYYMMDD | 2022-02-22 |
| PublicationDate_xml | – month: 02 year: 2022 text: 2022-02-22 day: 22 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: 1752 N St., N.W., Washington, DC |
| PublicationTitle | mBio |
| PublicationTitleAbbrev | mBio |
| PublicationTitleAlternate | mBio |
| PublicationYear | 2022 |
| Publisher | American Society for Microbiology |
| Publisher_xml | – name: American Society for Microbiology |
| References | e_1_3_2_26_2 e_1_3_2_28_2 e_1_3_2_41_2 e_1_3_2_20_2 e_1_3_2_43_2 e_1_3_2_22_2 e_1_3_2_45_2 e_1_3_2_24_2 e_1_3_2_47_2 e_1_3_2_9_2 e_1_3_2_16_2 e_1_3_2_37_2 e_1_3_2_7_2 e_1_3_2_18_2 e_1_3_2_39_2 e_1_3_2_10_2 e_1_3_2_31_2 e_1_3_2_5_2 e_1_3_2_12_2 e_1_3_2_33_2 e_1_3_2_3_2 e_1_3_2_14_2 e_1_3_2_35_2 e_1_3_2_27_2 e_1_3_2_48_2 e_1_3_2_29_2 e_1_3_2_40_2 e_1_3_2_21_2 e_1_3_2_42_2 e_1_3_2_23_2 e_1_3_2_44_2 e_1_3_2_25_2 e_1_3_2_46_2 National Research Council (e_1_3_2_49_2) 2011 e_1_3_2_15_2 e_1_3_2_38_2 e_1_3_2_8_2 e_1_3_2_17_2 e_1_3_2_6_2 e_1_3_2_19_2 e_1_3_2_30_2 e_1_3_2_32_2 e_1_3_2_51_2 e_1_3_2_11_2 e_1_3_2_34_2 e_1_3_2_4_2 e_1_3_2_13_2 e_1_3_2_36_2 e_1_3_2_2_2 Prophet EB (e_1_3_2_50_2) 1992 Meinhardt, J, Radke, J, Dittmayer, C, Franz, J, Thomas, C, Mothes, R, Laue, M, Schneider, J, Brünink, S, Greuel, S, Lehmann, M, Hassan, O, Aschman, T, Schumann, E, Chua, RL, Conrad, C, Eils, R, Stenzel, W, Windgassen, M, Rößler, L, Goebel, H-H, Gelderblom, HR, Martin, H, Nitsche, A, Schulz-Schaeffer, WJ, Hakroush, S, Winkler, MS, Tampe, B, Scheibe, F, Körtvélyessy, P, Reinhold, D, Siegmund, B, Kühl, AA, Elezkurtaj, S, Horst, D, Oesterhelweg, L, Tsokos, M, Ingold-Heppner, B, Stadelmann, C, Drosten, C, Corman, VM, Radbruch, H, Heppner, FL (B41) 2021; 24 Chu, H, Chan, JF-W, Yuen, TT-T, Shuai, H, Yuan, S, Wang, Y, Hu, B, Yip, CC-Y, Tsang, JO-L, Huang, X, Chai, Y, Yang, D, Hou, Y, Chik, KK-H, Zhang, X, Fung, AY-F, Tsoi, H-W, Cai, J-P, Chan, W-M, Ip, JD, Chu, AW-H, Zhou, J, Lung, DC, Kok, K-H, To, KK-W, Tsang, OT-Y, Chan, K-H, Yuen, K-Y (B39) 2020; 1 Bryche, B, St Albin, A, Murri, S, Lacôte, S, Pulido, C, Ar Gouilh, M, Lesellier, S, Servat, A, Wasniewski, M, Picard-Meyer, E, Monchatre-Leroy, E, Volmer, R, Rampin, O, Le Goffic, R, Marianneau, P, Meunier, N (B25) 2020; 89 Palahuta, HV, Fartushna, OY, Yevtushenko, SK, Hnepa, YY (B38) 2021; 74 Subbarao, K, McAuliffe, J, Vogel, L, Fahle, G, Fischer, S, Tatti, K, Packard, M, Shieh, W-J, Zaki, S, Murphy, B (B19) 2004; 78 Ye, Q, Wang, B, Mao, J (B7) 2020; 80 Imai, M, Iwatsuki-Horimoto, K, Hatta, M, Loeber, S, Halfmann, PJ, Nakajima, N, Watanabe, T, Ujie, M, Takahashi, K, Ito, M, Yamada, S, Fan, S, Chiba, S, Kuroda, M, Guan, L, Takada, K, Armbrust, T, Balogh, A, Furusawa, Y, Okuda, M, Ueki, H, Yasuhara, A, Sakai-Tagawa, Y, Lopes, TJS, Kiso, M, Yamayoshi, S, Kinoshita, N, Ohmagari, N, Hattori, SI, Takeda, M, Mitsuya, H, Krammer, F, Suzuki, T, Kawaoka, Y (B23) 2020; 117 Virhammar, J, Kumlien, E, Fällmar, D, Frithiof, R, Jackmann, S, Sköld, MK, Kadir, M, Frick, J, Lindeberg, J, Olivero-Reinius, H, Ryttlefors, M, Cunningham, JL, Wikström, J, Grabowska, A, Bondeson, K, Bergquist, J, Zetterberg, H, Rostami, E (B36) 2020; 95 (B48) 2011 Li, W, Moore, MJ, Vasilieva, N, Sui, J, Wong, SK, Berne, MA, Somasundaran, M, Sullivan, JL, Luzuriaga, K, Greenough, TC, Choe, H, Farzan, M (B12) 2003; 426 de Melo, GD, Lazarini, F, Levallois, S, Hautefort, C, Michel, V, Larrous, F, Verillaud, B, Apricio, C, Wagner, S, Gheusi, G, Kergoat, L, Kornobis, E, Donati, F, Cokelaer, T, Hervochon, R, Madec, Y, Roze, E, Salmon, D, Bourhy, H, Lecuit, M, Lledo, PM (B24) 2021; 13 Wan, Y, Shang, J, Graham, R, Baric, RS, Li, F (B17) 2020; 94 Shang, J, Ye, G, Shi, K, Wan, Y, Luo, C, Aihara, H, Geng, Q, Auerbach, A, Li, F (B13) 2020; 581 McCray, PB, Pewe, L, Wohlford-Lenane, C, Hickey, M, Manzel, L, Shi, L, Netland, J, Jia, HP, Halabi, C, Sigmund, CD, Meyerholz, DK, Kirby, P, Look, DC, Perlman, S (B27) 2007; 81 Natoli, S, Oliveira, V, Calabresi, P, Maia, LF, Pisani, A (B11) 2020; 27 Frontera, JA, Sabadia, S, Lalchan, R, Fang, T, Flusty, B, Millar-Vernetti, P, Snyder, T, Berger, S, Yang, D, Granger, A, Morgan, N, Patel, P, Gutman, J, Melmed, K, Agarwal, S, Bokhari, M, Andino, A, Valdes, E, Omari, M, Kvernland, A, Lillemoe, K, Chou, SH-Y, McNett, M, Helbok, R, Mainali, S, Fink, EL, Robertson, C, Schober, M, Suarez, JI, Ziai, W, Menon, D, Friedman, D, Friedman, D, Holmes, M, Huang, J, Thawani, S, Howard, J, Abou-Fayssal, N, Krieger, P, Lewis, A, Lord, AS, Zhou, T, Kahn, DE, Czeisler, BM, Torres, J, Yaghi, S, Ishida, K, Scher, E, de Havenon, A, Placantonakis, D, Liu, M, Wisniewski, T, Troxel, AB, Balcer, L, Galetta, S (B33) 2021; 96 Prophet, EB, Mills, B, Arrington, JB, Sobin, LH (B49) 1992 Golden, JW, Zeng, X, Cline, CR, Garrison, AR, White, LE, Fitzpatrick, CJ, Kwilas, SA, Bowling, PA, Fiallos, JO, Moore, JL, Sifford, WB, Ricks, KM, Mucker, EM, Smith, JM, Hooper, JW (B21) 2021; 102 Burks, SM, Rosas-Hernandez, H, Alejandro Ramirez-Lee, M, Cuevas, E, Talpos, JC (B42) 2021; 95 DosSantos, MF, Devalle, S, Aran, V, Capra, D, Roque, NR, Coelho-Aguiar, JDM, de Sampaio e Spohr, TCL, Subilhaga, JG, Pereira, CM, D'Andrea Meira, I, Niemeyer Soares Filho, P, Moura-Neto, V (B9) 2020; 14 Golden, JW, Cline, CR, Zeng, X, Garrison, AR, Carey, BD, Mucker, EM, White, LE, Shamblin, JD, Brocato, RL, Liu, J, Babka, AM, Rauch, HB, Smith, JM, Hollidge, BS, Fitzpatrick, C, Badger, CV, Hooper, JW (B20) 2020; 5 Winkler, ES, Bailey, AL, Kafai, NM, Nair, S, McCune, BT, Yu, J, Fox, JM, Chen, RE, Earnest, JT, Keeler, SP, Ritter, JH, Kang, L-I, Dort, S, Robichaud, A, Head, R, Holtzman, MJ, Diamond, MS (B29) 2020; 21 Salimi, S, Hamlyn, JM (B5) 2020; 75 Zheng, J, Wong, LR, Li, K, Verma, AK, Ortiz, ME, Wohlford-Lenane, C, Leidinger, MR, Knudson, CM, Meyerholz, DK, McCray, PB, Perlman, S (B28) 2021; 589 Liu, J, Babka, AM, Kearney, BJ, Radoshitzky, SR, Kuhn, JH, Zeng, X (B50) 2020; 5 Lan, J, Ge, J, Yu, J, Shan, S, Zhou, H, Fan, S, Zhang, Q, Shi, X, Wang, Q, Zhang, L, Wang, X (B16) 2020; 581 Fox, SE, Akmatbekov, A, Harbert, JL, Li, G, Quincy Brown, J, Vander Heide, RS (B43) 2020; 8 Harcourt, J, Tamin, A, Lu, X, Kamili, S, Sakthivel, SK, Murray, J, Queen, K, Tao, Y, Paden, CR, Zhang, J, Li, Y, Uehara, A, Wang, H, Goldsmith, C, Bullock, HA, Wang, L, Whitaker, B, Lynch, B, Gautam, R, Schindewolf, C, Lokugamage, KG, Scharton, D, Plante, JA, Mirchandani, D, Widen, SG, Narayanan, K, Makino, S, Ksiazek, TG, Plante, KS, Weaver, SC, Lindstrom, S, Tong, S, Menachery, VD, Thornburg, NJ (B47) 2020; 26 B46 Brocato, RL, Principe, LM, Kim, RK, Zeng, X, Williams, JA, Liu, Y, Li, R, Smith, JM, Golden, JW, Gangemi, D, Youssef, S, Wang, Z, Glanville, J, Hooper, JW (B26) 2020; 94 Chen, N, Zhou, M, Dong, X, Qu, J, Gong, F, Han, Y, Qiu, Y, Wang, J, Liu, Y, Wei, Y, Xia, J, Yu, T, Zhang, X, Zhang, L (B1) 2020; 395 Chan, JFW, Zhang, AJ, Yuan, S, Poon, VKM, Chan, CCS, Lee, ACY, Chan, WM, Fan, Z, Tsoi, HW, Wen, L, Liang, R, Cao, J, Chen, Y, Tang, K, Luo, C, Cai, JP, Kok, KH, Chu, H, Chan, KH, Sridhar, S, Chen, Z, Chen, H, To, KKW, Yuen, KY (B22) 2020; 71 Hanafi, R, Roger, PA, Perin, B, Kuchcinski, G, Deleval, N, Dallery, F, Michel, D, Hacein-Bey, L, Pruvo, JP, Outteryck, O, Constans, JM (B34) 2020; 41 Song, E, Zhang, C, Israelow, B, Lu-Culligan, A, Prado, AV, Skriabine, S, Lu, P, Weizman, OE, Liu, F, Dai, Y, Szigeti-Buck, K, Yasumoto, Y, Wang, G, Castaldi, C, Heltke, J, Ng, E, Wheeler, J, Alfajaro, MM, Levavasseur, E, Fontes, B, Ravindra, NG, Van Dijk, D, Mane, S, Gunel, M, Ring, A, Kazmi, SAJ, Zhang, K, Wilen, CB, Horvath, TL, Plu, I, Haik, S, Thomas, JL, Louvi, A, Farhadian, SF, Huttner, A, Seilhean, D, Renier, N, Bilguvar, K, Iwasaki, A (B31) 2021; 218 Wrapp, D, Wang, N, Corbett, KS, Goldsmith, JA, Hsieh, C-L, Abiona, O, Graham, BS, McLellan, JS (B15) 2020; 367 Zhou, P, Yang, X-L, Wang, X-G, Hu, B, Zhang, L, Zhang, W, Si, H-R, Zhu, Y, Li, B, Huang, C-L, Chen, H-D, Chen, J, Luo, Y, Guo, H, Jiang, R-D, Liu, M-Q, Chen, Y, Shen, X-R, Wang, X, Zheng, X-S, Zhao, K, Chen, Q-J, Deng, F, Liu, L-L, Yan, B, Zhan, F-X, Wang, Y-Y, Xiao, G-F, Shi, Z-L (B2) 2020; 579 Coperchini, F, Chiovato, L, Croce, L, Magri, F, Rotondi, M (B30) 2020; 53 Ellul, MA, Benjamin, L, Singh, B, Lant, S, Michael, BD, Easton, A, Kneen, R, Defres, S, Sejvar, J, Solomon, T (B32) 2020; 19 Hoffmann, M, Kleine-Weber, H, Schroeder, S, Krüger, N, Herrler, T, Erichsen, S, Schiergens, TS, Herrler, G, Wu, N-H, Nitsche, A, Müller, MA, Drosten, C, Pöhlmann, S (B14) 2020; 181 Vardhana, SA, Wolchok, JD (B8) 2020; 217 Reichard, RR, Kashani, KB, Boire, NA, Constantopoulos, E, Guo, Y, Lucchinetti, CF (B35) 2020; 140 Haslbauer, JD, Tzankov, A, Mertz, KD, Schwab, N, Nienhold, R, Twerenbold, R, Leibundgut, G, Stalder, AK, Matter, M, Glatz, K (B44) 2021; 7 Barnes, BJ, Adrover, JM, Baxter-Stoltzfus, A (B4) 2020; 217 Cajanding, RJM (B45) 2021; 32 Bocci, T, Bulfamante, G, Campiglio, L, Coppola, S, Falleni, M, Chiumello, D, Priori, A (B40) 2021; 268 Tang, D, Comish, P, Kang, R (B6) 2020; 16 Yang, X, Yu, Y, Xu, J, Shu, H, Xia, J, Liu, H, Wu, Y, Zhang, L, Yu, Z, Fang, M, Yu, T, Wang, Y, Pan, S, Zou, X, Yuan, S, Shang, Y (B3) 2020; 8 Hopkins, C, Surda, P, Whitehead, E, Kumar, BN (B10) 2020; 49 Gretebeck, LM, Subbarao, K (B18) 2015; 13 Lewis, A, Jain, R, Frontera, J, Placantonakis, DG, Galetta, S, Balcer, L, Melmed, KR (B37) 2021; 31 |
| References_xml | – ident: e_1_3_2_7_2 doi: 10.1371/journal.ppat.1008536 – ident: e_1_3_2_31_2 doi: 10.1016/j.cytogfr.2020.05.003 – ident: e_1_3_2_46_2 doi: 10.4037/aacnacc2021302 – ident: e_1_3_2_32_2 doi: 10.1084/jem.20202135 – ident: e_1_3_2_34_2 doi: 10.1212/WNL.0000000000010979 – ident: e_1_3_2_37_2 doi: 10.1212/WNL.0000000000010250 – ident: e_1_3_2_33_2 doi: 10.1016/S1474-4422(20)30221-0 – ident: e_1_3_2_13_2 doi: 10.1038/nature02145 – ident: e_1_3_2_23_2 doi: 10.1093/cid/ciaa325 – ident: e_1_3_2_21_2 doi: 10.1172/jci.insight.142032 – ident: e_1_3_2_8_2 doi: 10.1016/j.jinf.2020.03.037 – ident: e_1_3_2_4_2 doi: 10.1016/S2213-2600(20)30079-5 – ident: e_1_3_2_35_2 doi: 10.3174/ajnr.A6651 – ident: e_1_3_2_24_2 doi: 10.1073/pnas.2009799117 – ident: e_1_3_2_11_2 doi: 10.1186/s40463-020-00423-8 – ident: e_1_3_2_16_2 doi: 10.1126/science.abb2507 – ident: e_1_3_2_30_2 doi: 10.1038/s41590-020-0778-2 – ident: e_1_3_2_39_2 doi: 10.36740/WLek202104144 – ident: e_1_3_2_25_2 doi: 10.1126/scitranslmed.abf8396 – ident: e_1_3_2_12_2 doi: 10.1111/ene.14277 – ident: e_1_3_2_2_2 doi: 10.1016/S0140-6736(20)30211-7 – ident: e_1_3_2_43_2 doi: 10.1016/j.bbi.2020.12.031 – ident: e_1_3_2_45_2 doi: 10.1002/cjp2.212 – ident: e_1_3_2_9_2 doi: 10.1084/jem.20200678 – ident: e_1_3_2_28_2 doi: 10.1128/JVI.02012-06 – ident: e_1_3_2_40_2 doi: 10.1016/S2666-5247(20)30004-5 – volume-title: Guide for the care and use of laboratory animals year: 2011 ident: e_1_3_2_49_2 – ident: e_1_3_2_20_2 doi: 10.1128/jvi.78.7.3572-3577.2004 – ident: e_1_3_2_29_2 doi: 10.1038/s41586-020-2943-z – ident: e_1_3_2_22_2 doi: 10.1099/jgv.0.001599 – ident: e_1_3_2_15_2 doi: 10.1016/j.cell.2020.02.052 – ident: e_1_3_2_42_2 doi: 10.1038/s41593-020-00758-5 – ident: e_1_3_2_18_2 doi: 10.1128/JVI.00127-20 – ident: e_1_3_2_48_2 doi: 10.3201/eid2606.200516 – ident: e_1_3_2_17_2 doi: 10.1038/s41586-020-2180-5 – ident: e_1_3_2_3_2 doi: 10.1038/s41586-020-2012-7 – ident: e_1_3_2_47_2 doi: 10.1101/2021.07.26.453840 – ident: e_1_3_2_26_2 doi: 10.1016/j.bbi.2020.06.032 – ident: e_1_3_2_6_2 doi: 10.1093/gerona/glaa149 – ident: e_1_3_2_19_2 doi: 10.1016/j.coviro.2015.06.009 – volume-title: Laboratory methods for histotechnology. year: 1992 ident: e_1_3_2_50_2 – ident: e_1_3_2_27_2 doi: 10.1128/JVI.01683-20 – ident: e_1_3_2_36_2 doi: 10.1007/s00401-020-02166-2 – ident: e_1_3_2_41_2 doi: 10.1007/s00415-021-10474-0 – ident: e_1_3_2_5_2 doi: 10.1084/jem.20200652 – ident: e_1_3_2_44_2 doi: 10.1016/S2213-2600(20)30243-5 – ident: e_1_3_2_10_2 doi: 10.3389/fnana.2020.00037 – ident: e_1_3_2_38_2 doi: 10.1111/jon.12880 – ident: e_1_3_2_51_2 doi: 10.1172/jci.insight.139042 – ident: e_1_3_2_14_2 doi: 10.1038/s41586-020-2179-y – volume: 94 year: 2020 ident: B26 article-title: Disruption of adaptive immunity enhances disease in SARS-CoV-2-infected Syrian hamsters publication-title: J Virol doi: 10.1128/JVI.01683-20 – volume: 218 year: 2021 ident: B31 article-title: Neuroinvasion of SARS-CoV-2 in human and mouse brain publication-title: J Exp Med doi: 10.1084/jem.20202135 – volume: 71 start-page: 2428 year: 2020 end-page: 2446 ident: B22 article-title: Simulation of the clinical and pathological manifestations of coronavirus disease 2019 (COVID-19) in a golden Syrian hamster model: implications for disease pathogenesis and transmissibility publication-title: Clin Infect Dis doi: 10.1093/cid/ciaa325 – volume: 89 start-page: 579 year: 2020 end-page: 586 ident: B25 article-title: Massive transient damage of the olfactory epithelium associated with infection of sustentacular cells by SARS-CoV-2 in golden Syrian hamsters publication-title: Brain Behav Immun doi: 10.1016/j.bbi.2020.06.032 – volume: 217 year: 2020 ident: B4 article-title: Targeting potential drivers of COVID-19: neutrophil extracellular traps publication-title: J Exp Med doi: 10.1084/jem.20200652 – volume: 581 start-page: 215 year: 2020 end-page: 220 ident: B16 article-title: Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor publication-title: Nature doi: 10.1038/s41586-020-2180-5 – volume: 8 start-page: 681 year: 2020 end-page: 686 ident: B43 article-title: Pulmonary and cardiac pathology in African American patients with COVID-19: an autopsy series from New Orleans publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(20)30243-5 – volume: 181 start-page: 271 year: 2020 end-page: 280.E8 ident: B14 article-title: SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor publication-title: Cell doi: 10.1016/j.cell.2020.02.052 – ident: B46 article-title: Gilliland T , Liu Y , Li R , Dunn M , Cottle E , Terada Y , Ryckman Z , Alcorn M , Vasilatos S , Lundy J , Larson D , Wu H , Luke T , Bausch C , Egland K , Sullivan E , Wang Z , Klimstra WB . 2021 . Protection of human ACE2 transgenic Syrian hamsters from SARS CoV-2 variants by human polyclonal IgG from hyper-immunized transchromosomic bovines . bioRxiv . doi: 10.1101/2021.07.26.453840 . – volume: 395 start-page: 507 year: 2020 end-page: 513 ident: B1 article-title: Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study publication-title: Lancet doi: 10.1016/S0140-6736(20)30211-7 – volume: 117 start-page: 16587 year: 2020 end-page: 16595 ident: B23 article-title: Syrian hamsters as a small animal model for SARS-CoV-2 infection and countermeasure development publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.2009799117 – volume: 21 start-page: 1327 year: 2020 end-page: 1335 ident: B29 article-title: SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function publication-title: Nat Immunol doi: 10.1038/s41590-020-0778-2 – volume: 81 start-page: 813 year: 2007 end-page: 821 ident: B27 article-title: Lethal infection of K18-hACE2 mice infected with severe acute respiratory syndrome coronavirus publication-title: J Virol doi: 10.1128/JVI.02012-06 – volume: 1 start-page: e14 year: 2020 end-page: e23 ident: B39 article-title: Comparative tropism, replication kinetics, and cell damage profiling of SARS-CoV-2 and SARS-CoV with implications for clinical manifestations, transmissibility, and laboratory studies of COVID-19: an observational study publication-title: Lancet Microbe doi: 10.1016/S2666-5247(20)30004-5 – volume: 96 start-page: e575 year: 2021 end-page: e586 ident: B33 article-title: A prospective study of neurologic disorders in hospitalized patients with COVID-19 in New York City publication-title: Neurology doi: 10.1212/WNL.0000000000010979 – volume: 140 start-page: 1 year: 2020 end-page: 6 ident: B35 article-title: Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology publication-title: Acta Neuropathol doi: 10.1007/s00401-020-02166-2 – volume: 14 start-page: 37 year: 2020 ident: B9 article-title: Neuromechanisms of SARS-CoV-2: a review publication-title: Front Neuroanat doi: 10.3389/fnana.2020.00037 – volume: 32 start-page: 169 year: 2021 end-page: 187 ident: B45 article-title: Comprehensive review of cardiovascular involvement in COVID-19 publication-title: AACN Adv Crit Care doi: 10.4037/aacnacc2021302 – volume: 8 start-page: 475 year: 2020 end-page: 481 ident: B3 article-title: Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(20)30079-5 – volume: 24 start-page: 168 year: 2021 end-page: 175 ident: B41 article-title: Olfactory transmucosal SARS-CoV-2 invasion as a port of central nervous system entry in individuals with COVID-19 publication-title: Nat Neurosci doi: 10.1038/s41593-020-00758-5 – volume: 268 start-page: 3598 year: 2021 end-page: 3600 ident: B40 article-title: Brainstem clinical and neurophysiological involvement in COVID-19 publication-title: J Neurol doi: 10.1007/s00415-021-10474-0 – volume: 95 start-page: 7 year: 2021 end-page: 14 ident: B42 article-title: Can SARS-CoV-2 infect the central nervous system via the olfactory bulb or the blood-brain barrier? publication-title: Brain Behav Immun doi: 10.1016/j.bbi.2020.12.031 – volume: 13 year: 2021 ident: B24 article-title: COVID-19-related anosmia is associated with viral persistence and inflammation in human olfactory epithelium and brain infection in hamsters publication-title: Sci Transl Med doi: 10.1126/scitranslmed.abf8396 – volume: 53 start-page: 25 year: 2020 end-page: 32 ident: B30 article-title: The cytokine storm in COVID-19: an overview of the involvement of the chemokine/chemokine-receptor system publication-title: Cytokine Growth Factor Rev doi: 10.1016/j.cytogfr.2020.05.003 – volume: 41 start-page: 1384 year: 2020 end-page: 1387 ident: B34 article-title: COVID-19 neurologic complication with CNS vasculitis-like pattern publication-title: AJNR Am J Neuroradiol doi: 10.3174/ajnr.A6651 – volume: 49 start-page: 26 year: 2020 ident: B10 article-title: Early recovery following new onset anosmia during the COVID-19 pandemic—an observational cohort study publication-title: J Otolaryngol Head Neck Surg doi: 10.1186/s40463-020-00423-8 – volume: 78 start-page: 3572 year: 2004 end-page: 3577 ident: B19 article-title: Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus in the respiratory tract of mice publication-title: J Virol doi: 10.1128/jvi.78.7.3572-3577.2004 – volume: 7 start-page: 326 year: 2021 end-page: 337 ident: B44 article-title: Characterisation of cardiac pathology in 23 autopsies of lethal COVID-19 publication-title: J Pathol Clin Res doi: 10.1002/cjp2.212 – volume: 75 start-page: e34 year: 2020 end-page: e41 ident: B5 article-title: COVID-19 and crosstalk with the hallmarks of aging publication-title: J Gerontol A Biol Sci Med Sci doi: 10.1093/gerona/glaa149 – volume: 19 start-page: 767 year: 2020 end-page: 783 ident: B32 article-title: Neurological associations of COVID-19 publication-title: Lancet Neurol doi: 10.1016/S1474-4422(20)30221-0 – volume: 367 start-page: 1260 year: 2020 end-page: 1263 ident: B15 article-title: Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation publication-title: Science doi: 10.1126/science.abb2507 – volume: 102 start-page: 001599 year: 2021 ident: B21 article-title: Human convalescent plasma protects K18-hACE2 mice against severe respiratory disease publication-title: J Gen Virol doi: 10.1099/jgv.0.001599 – volume: 74 start-page: 1045 year: 2021 end-page: 1049 ident: B38 article-title: Acute transverse myelitis as a neurological complication of Covid-19: a case report publication-title: Wiad Lek doi: 10.36740/WLek202104144 – volume: 31 start-page: 826 year: 2021 end-page: 848 ident: B37 article-title: COVID-19 associated brain/spinal cord lesions and leptomeningeal enhancement: a meta-analysis of the relationship to CSF SARS-CoV-2 publication-title: J Neuroimaging doi: 10.1111/jon.12880 – volume: 579 start-page: 270 year: 2020 end-page: 273 ident: B2 article-title: A pneumonia outbreak associated with a new coronavirus of probable bat origin publication-title: Nature doi: 10.1038/s41586-020-2012-7 – volume: 26 start-page: 1266 year: 2020 end-page: 1273 ident: B47 article-title: Severe acute respiratory syndrome coronavirus 2 from patient with coronavirus disease, United States publication-title: Emerg Infect Dis doi: 10.3201/eid2606.200516 – year: 1992 ident: B49 publication-title: Laboratory methods for histotechnology. ;Armed Forces Institute of Pathology ;Washington, DC – volume: 5 year: 2020 ident: B20 article-title: Human angiotensin-converting enzyme 2 transgenic mice infected with SARS-CoV-2 develop severe and fatal respiratory disease publication-title: JCI Insight doi: 10.1172/jci.insight.142032 – volume: 13 start-page: 123 year: 2015 end-page: 129 ident: B18 article-title: Animal models for SARS and MERS coronaviruses publication-title: Curr Opin Virol doi: 10.1016/j.coviro.2015.06.009 – volume: 80 start-page: 607 year: 2020 end-page: 613 ident: B7 article-title: The pathogenesis and treatment of the “cytokine storm” in COVID-19 publication-title: J Infect doi: 10.1016/j.jinf.2020.03.037 – year: 2011 ident: B48 publication-title: Guide for the care and use of laboratory animals ;8th ed ;National Academies Press ;Washington, DC – volume: 217 year: 2020 ident: B8 article-title: The many faces of the anti-COVID immune response publication-title: J Exp Med doi: 10.1084/jem.20200678 – volume: 5 year: 2020 ident: B50 article-title: Molecular detection of SARS-CoV-2 in formalin fixed paraffin embedded specimens publication-title: JCI Insight doi: 10.1172/jci.insight.139042 – volume: 581 start-page: 221 year: 2020 end-page: 224 ident: B13 article-title: Structural basis of receptor recognition by SARS-CoV-2 publication-title: Nature doi: 10.1038/s41586-020-2179-y – volume: 16 year: 2020 ident: B6 article-title: The hallmarks of COVID-19 disease publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1008536 – volume: 426 start-page: 450 year: 2003 end-page: 454 ident: B12 article-title: Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus publication-title: Nature doi: 10.1038/nature02145 – volume: 94 year: 2020 ident: B17 article-title: Receptor recognition by the novel coronavirus from Wuhan: an analysis based on decade-long structural studies of SARS coronavirus publication-title: J Virol doi: 10.1128/JVI.00127-20 – volume: 95 start-page: 445 year: 2020 end-page: 449 ident: B36 article-title: Acute necrotizing encephalopathy with SARS-CoV-2 RNA confirmed in cerebrospinal fluid publication-title: Neurology doi: 10.1212/WNL.0000000000010250 – volume: 589 start-page: 603 year: 2021 end-page: 607 ident: B28 article-title: COVID-19 treatments and pathogenesis including anosmia in K18-hACE2 mice publication-title: Nature doi: 10.1038/s41586-020-2943-z – volume: 27 start-page: 1764 year: 2020 end-page: 1773 ident: B11 article-title: Does SARS-CoV-2 invade the brain? Translational lessons from animal models publication-title: Eur J Neurol doi: 10.1111/ene.14277 |
| SSID | ssj0000331830 |
| Score | 2.402484 |
| Snippet | The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe,... The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to... ABSTRACT The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is... |
| SourceID | doaj pubmedcentral proquest asm2 pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e0290621 |
| SubjectTerms | Angiotensin-Converting Enzyme 2 Animals cardiac lesions COVID-19 - pathology Cricetinae Disease Models, Animal Host-Microbial Interactions Humans K18-hACE2 Lung - pathology Mice Mice, Transgenic nasal cavity Peptidyl-Dipeptidase A Research Article SARS-CoV-2 transgenic hamsters |
| SummonAdditionalLinks | – databaseName: American Society for Microbiology Open Access dbid: AAUOK link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwELemTUi8IMZn2EBGIJ7IqB3Hdh7D1qkCARKlaG-WndhdJZqMtdM2_nru8qV1YhJ9SZVcnMR3Z_9s3_1MyNvEpWUA5B1br4tYqAD_eOpg1Kqt48JlTGCC85evcjITn07Sky3C-1yYrgZXB3a1bBbyB8_m-sPSLeqDERKUx5g7vpPyTIAz7uT57NvnYWZllKCdjnpCzdv3QdsLZfONfqih6_8XxrwdKnmj7zl-SB50oJHmrZZ3yZavHpF77TaS14_J74ldIt_Bio6v2rjWak6b2XmaV_NF3QSpV_EhBpgjacCcjqs_10tPOe1ihugUjueeHrXLNTSAddSXjeTVWY2TiHRd02n-fQql_Iz5EzI7Hv84nMTdVgqxBQ9dxwWy9NigwMFtar3LSsUC_Ly3gA-lZyNXaFwdLh104cGFROmsZEFpEXgh0-Qp2a7qyj8n1EkoRCYqC0IKC-UFGMalSWCFSlJV8Ii8wfo1vSZNM8zg2qAWTKMFw1lE3vfVb4qOjRw3xfh1l_i7QfyspeG4S_Aj6nIQQvbs5gTYkumc0aiSOYDrklv4BB2chnZOFIwjmZ8UTEXkdW8JBrwNl1Bs5euLleES4KrEYWVEnrWWMTwqAWidAACLiNqwmY132bxSLU4bRm8NzaaQ6Yv_qro9cp9jDgbm1fN9sr0-v_AvARmt3avOFf4CoFIKiw priority: 102 providerName: American Society for Microbiology – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lj9MwELZQJSQuiDfhJSMQJ8LWj9jusSxdVUhwoCzam2UndrcSdZZtV-zy65lx0qpFrLiQS6Jk5Fj2N_E38fgzIa-Fr5oIzLt0wdSl1BGueOUhajXOc-lHTOIC50-f1fRYfjypTna2-sKcsE4euGu4A90wD9RKcSeVNNEbwKSsGUfhNSVZXkcOY95OMJW_wQKxOtyIanJzsPSL9t0Qxc1L1AUduNWS741FWbL_bzzzz3TJnfHn6A653RNHOu4qfJfcCOkeudltJXl1n_yYuiVqHqzo5LLLbU1zmv_Q03GaL9qcqJ7KQ0wyR-GAOZ2kX1fLQDnt84boDM7ngX7opmxoBIS0P7Pl5VmLPxLpuqWz8ZcZlPKt5A_I8dHk6-G07LdTKB146bqsUanHRQ1O7ioX_KjRLMIRggOOqAIb-trgDHHjYRiPPgptRg2L2sjIa1WJh2SQ2hQeE-oVFKKEHkXoFAflRQjlKhFZrUWla16QV9i-tveHlc2hBjcWe8HmXrCcFeTtpvlt3SuS48YY368zf7M1P-ukOK4zfI99uTVCBe18A3Ble1zZf-GqIC83SLDgcTiN4lJoL1aWK6CsCkPLgjzqkLF9lQB6LYCEFUTvYWavLvtP0uI0q3ob-HRKVT35H5V_Sm5xXKaBS-_5MzJYn1-E50Ce1v5F9pPfUWUU6g priority: 102 providerName: Directory of Open Access Journals |
| Title | Hamsters Expressing Human Angiotensin-Converting Enzyme 2 Develop Severe Disease following Exposure to SARS-CoV-2 |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/35073750 https://journals.asm.org/doi/10.1128/mbio.02906-21 https://www.proquest.com/docview/2622660149 https://pubmed.ncbi.nlm.nih.gov/PMC8787465 https://doaj.org/article/7d1b81b62a4648fb80734c1228596417 |
| Volume | 13 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwELfQJiReEN-Ej8oIxBMZtZPY7gNCYXRUoIFEKeqbZSd2V2lNtrYTLX89d05a6LRJ9KGtUstp7PPd7-y73xHyKrFZ6QF5x8apIk6lh288s-C1KmN5anssxQTn469iMEo_j7PxX0qhdgAXV7p2WE9qND89WJ2v38OCf9ckwKi3MzutD7rIWx5jSvk-GCWJxQyOW6QflHKCwos7LmDjurEEnLFh3LzcAyhns5jxHUMV-PyvAqGXYyn_MU5Hd8jtFlXSvBGDu-SGq-6Rm02dyfV9cj4wMyREWND-qgl8rSY0bN_TvJpM6xDFXsWHGIGOrAIT2q9-r2eOctoGFdEhfM4d_dic51AP4lP_Ci1XZzXuMtJlTYf59yH08jPmD8joqP_jcBC3tRZiA0t4GRdI42O8BA1gMuNsr5TMw8s5AwBSONa1hcLj49KCjffWJ1L1SualSj0vRJY8JHtVXbnHhFoBnYhE9nwqUgP9efDzssSzQiaZLHhEXuL46s1c6-CHcKVxFnSYBc1ZRN5shl8XLV05Vs04va75623zs4an47qGH3Aut42QXjtcqOcT3a5WLUtmAc8LbuARlLcKFGFaMI5sfwKkKyIvNpKgYTniGYupXH2x0FwAnhXod0bkUSMZ21slgL0TQGgRkTsys_Nfdn-ppieB8luBXk1F9uQ_7vuU3OKYooFp9_wZ2VvOL9xzAE5L2yH7eT769qUTNh7g_dOYdcIy-QMAehg- |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3dT9swELcQaNpe0L6XfXrax9PCaiex3Yc9ZFBUVmDSSifejJ3apRNNGCmC7g_a37m7JK1WNKS9kJdEyclJ7Lvzne_8O0LeRjYZerC8Q-NUFsbSwxVPLHitylge2zaLcYPz3r7oDuIvh8nhCvk93wvzA-vynpQbppxUcXwUbFyIbuoRqo8TOy42WghSHnLWJFP23OwCXLXy084WjOs7zrc7B5vdsKkmEBpg0mmYIVCN8RJ43CTG2fZQMg-HcwZMJOFYy2YKA6RDC7OYtz6Sqj1kXqrY80xgdQhQ9WsYpwQnby1NB197i9WcVoSy0ZqDeF79TtD38EN8ae6rSgT8y669mp7513y3fZesN4YqTWvOukdWXH6f3KpLV84ekJ9dM0GMhZJ2Lutc2nxEq4gATfPRuKgS4_NwE5PaEahgRDv5r9nEUU6bPCXah_OZo1t1iIh64MjioqK8PC1w4ZJOC9pPv_Whle8hf0gGN9Lhj8hqXuTuCaFWQCMikm0fi9hAex5cxyTyLJNRIjMekDfYv7qRv1JXrg1XGkdBV6OgOQvIh3n366xBQMdCHCfXkb9fkJ_W0B_XEX7GsVwQIWJ3dQMYWDcKQMshs-AiCG7gF5S3CnRrnDGOAIIiZjIgr-ecoEHCMWxjclecl5oLMJEFurIBeVxzxuJVEZjzERh9AZFLPLP0LctP8vFxhSKuQFXHInn6X133itzuHuzt6t2d_d4zcofjHhDc18-fk9Xp2bl7AZbZ1L5sxIKSo5uWxD-710oK |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3db9MwELemTiBeEN-ETyM-nsioncR2H3gIa6uOwkCUTnszdmKXSjQpa6et_EH8nZydpFqnTeJleWnUntzkfHe-851_h9CrSCe5Bc87VEZkYcwt3NFEQ9QqlKax7pDYHXD-vM8G4_jjYXK4hf42Z2FqDi521GLmE_lOs-e5rfsRinczPS132g6kPKSkLqYcmtUJhGqL93tdmNfXlPZ733cHYd1NIFQgpMswc0A1ynKQcZUoozs5JxYuYxS4SMyQts6ES5DmGlYxq23ERScnlovY0oy57hBg6rd9YqyFttN0_GW43s1pR0432g2I5_nnBHsP70M31j7fIuAiv_Z8eeaZ9a5_C92sHVWcVpJ1G22Z4g66VrWuXN1Fvwdq5jAWFrh3WtXSFhPsMwI4LSbT0hfGF-GuK2p3QAUT3Cv-rGYGU1zXKeERfB4Z3K1SRNiCRJYnnvJ0XrqNS7ws8Sj9NoJRDkJ6D42vhOH3UasoC_MQYc1gEBbxjo1ZrGA8C6FjElmS8SjhGQ3QS8df2UiP9KENFdLNgvSzICkJ0NuG_TKrEdBdI45fl5G_WZPPK-iPywg_uLlcEznEbv8FyK-sDYDkOdEQIjCq4BWE1QJsa5wR6gAEWUx4gF40kiBBw13aRhWmPF5IysBFZi6UDdCDSjLWfxWBOx-B0xcgviEzG8-y-Usx_elRxAWY6pglj_6Ldc_R9a_dvvy0tz98jG5QdwTEV64_Qa3l0bF5Co7ZUj-rtQKjH1etiP8ARQpJow |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Hamsters+Expressing+Human+Angiotensin-Converting+Enzyme+2+Develop+Severe+Disease+following+Exposure+to+SARS-CoV-2&rft.jtitle=mBio&rft.au=Golden%2C+Joseph+W&rft.au=Li%2C+Rong&rft.au=Cline%2C+Curtis+R&rft.au=Zeng%2C+Xiankun&rft.date=2022-02-22&rft.issn=2150-7511&rft.eissn=2150-7511&rft.volume=13&rft.issue=1&rft.spage=e0290621&rft_id=info:doi/10.1128%2Fmbio.02906-21&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2150-7511&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2150-7511&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2150-7511&client=summon |