ArticleJCI insight2021
L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The trial behind it
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- The Scavenger Function of LSECs, a Regulator of Liver Diseases.Current issues in molecular biology · 2026Review
- Bridging Viral Glycobiology and Lectin Biotechnology for Antiviral and Diagnostic Strategies.ACS bio & med chem Au · 2025Review
- N-glycosylation of the PEDV spike protein modulates viral replication and pathogenicity.Veterinary research · 2025Article
- MCP-1 Reduction by L-SIGN Expression in Dengue Virus-Infected Liver Endothelial Cells.Viruses · 2025Article
- TMPRSS2 as a Key Player in Viral Pathogenesis: Influenza and Coronaviruses.Biomolecules · 2025Review
- Challenging the notion of endothelial infection by SARS-CoV-2: insights from the current scientific evidence.Frontiers in immunology · 2025Article
- Virus-specific host responses and gene signatures following infection with major SARS-CoV-2 variants of concern: role of ZBP1 in viral clearance and lung inflammation.Frontiers in immunology · 2025Article
- SARS-CoV-2-associated lymphopenia: possible mechanisms and the role of CD147.Cell communication and signaling : CCS · 2024Review
- Interleukin-7-based identification of liver lymphatic endothelial cells reveals their unique structural features.JHEP reports : innovation in hepatology · 2024Article
- Article
- Hydroxypropyl-β-Cyclodextrin Depletes Membrane Cholesterol and Inhibits SARS-CoV-2 Entry into HEK293T-ACEPathogens (Basel, Switzerland) · 2023Article
- Powerful Avidity with a Limited Valency for Virus-Attachment Blockers on DC-SIGN: Combining Chelation and Statistical Rebinding with Structural Plasticity of the Receptor.ACS central science · 2023Article
- Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies.Acta pharmacologica Sinica · 2023Review
- Long COVID and hypertension-related disorders: a report from the Japanese Society of Hypertension Project Team on COVID-19.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Review
- LRRC15 mediates an accessory interaction with the SARS-CoV-2 spike protein.PLoS biology · 2023Article
- Infection of liver sinusoidal endothelial cells with Muromegalovirus muridbeta1 involves binding to neuropilin-1 and is dynamin-dependent.Frontiers in cellular and infection microbiology · 2023Article
- SARS-CoV-2 Receptors and Their Involvement in Cell Infection.Biochemistry (Moscow) Supplement. Series A, Membrane and cell biology · 2023Article
- Liver injury in COVID-19: A minireview.World journal of gastroenterology · 2022Review
- COVID-19-associated liver injury: Clinical characteristics, pathophysiological mechanisms and treatment management.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Recent advances in passive immunotherapies for COVID-19: The Evidence-Based approaches and clinical trials.International immunopharmacology · 2022Review
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.