L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report...

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Published in:JCI insight Vol. 6; no. 14
Main Authors: Kondo, Yuji, Larabee, Jason L., Gao, Liang, Shi, Huiping, Shao, Bojing, Hoover, Christopher M., McDaniel, J. Michael, Ho, Yen-Chun, Silasi-Mansat, Robert, Archer-Hartmann, Stephanie A., Azadi, Parastoo, Srinivasan, R. Sathish, Rezaie, Alireza R., Borczuk, Alain, Laurence, Jeffrey C., Lupu, Florea, Ahamed, Jasimuddin, McEver, Rodger P., Papin, James F., Yu, Zhongxin, Xia, Lijun
Format: Journal Article
Language:English
Published: Ann Arbor American Society for Clinical Investigation 22.07.2021
American Society for Clinical investigation
Subjects:
ACE2
Amino acids
Angiotensin-converting enzyme 2
Autopsies
Autopsy
Calcium
Calcium channels (C-type)
Cell biology
Clotting
Coagulation factors
Confocal microscopy
Coronaviruses
COVID-19
Endothelial cells
Flow cytometry
Glycosylation
Hepatocytes
Infections
Lectins
Liver
Lymph nodes
Lymphatic system
Mannose
N-glycans
Pandemics
Polysaccharides
Proteins
Severe acute respiratory syndrome coronavirus 2
Spike protein
Thrombosis
Vascular biology
Viruses
ISSN:2379-3708, 2379-3708
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Abstract Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose–type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN–expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2–type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19–associated coagulopathy.
AbstractList Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose–type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN–expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2–type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19–associated coagulopathy.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose-type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN-expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2-type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19-associated coagulopathy.Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose-type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN-expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2-type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19-associated coagulopathy.
Author Laurence, Jeffrey C.
Yu, Zhongxin
Hoover, Christopher M.
Silasi-Mansat, Robert
McEver, Rodger P.
Gao, Liang
Papin, James F.
McDaniel, J. Michael
Ahamed, Jasimuddin
Shi, Huiping
Xia, Lijun
Larabee, Jason L.
Kondo, Yuji
Srinivasan, R. Sathish
Archer-Hartmann, Stephanie A.
Shao, Bojing
Borczuk, Alain
Lupu, Florea
Ho, Yen-Chun
Azadi, Parastoo
Rezaie, Alireza R.
AuthorAffiliation 5 Department of Pathology and Laboratory Medicine and
7 Department of Pathology and
1 Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA
3 Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
2 Department of Microbiology and Immunology and
4 Complex Carbohydrate Research Center, University of Georgia, Athens, Georgia, USA
6 Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, New York, USA
8 Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
AuthorAffiliation_xml – name: 3 Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
– name: 4 Complex Carbohydrate Research Center, University of Georgia, Athens, Georgia, USA
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– name: 1 Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA
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2021 Kondo et al. 2021 Kondo et al.
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SubjectTerms ACE2
Amino acids
Angiotensin-converting enzyme 2
Autopsies
Autopsy
Calcium
Calcium channels (C-type)
Cell biology
Clotting
Coagulation factors
Confocal microscopy
Coronaviruses
COVID-19
Endothelial cells
Flow cytometry
Glycosylation
Hepatocytes
Infections
Lectins
Liver
Lymph nodes
Lymphatic system
Mannose
N-glycans
Pandemics
Polysaccharides
Proteins
Severe acute respiratory syndrome coronavirus 2
Spike protein
Thrombosis
Vascular biology
Viruses
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