AI Article Synopsis

  • COVID-19, caused by SARS-CoV-2, continues to impact global health, with severe cases leading to multiple organ dysfunction.
  • Researchers discovered that the receptor L-SIGN interacts with the SARS-CoV-2 spike protein and is present in specific endothelial cells, like liver sinusoidal endothelial cells (LSECs), which can facilitate infection.
  • Increased levels of clotting factors vWF and FVIII were found in LSECs from COVID-19 patients, suggesting that L-SIGN plays a role in the coagulopathy associated with the disease.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8410055PMC
http://dx.doi.org/10.1172/jci.insight.148999DOI Listing

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