Kidney organoids reveal redundancy in viral entry pathways during ACE2-dependent SARS-CoV-2 infection
Summary
Utilizing a human iPSC-derived kidney organoid model with improved proximal tubule (PT) maturity, we identified the mechanism of SARS-CoV-2 entry in renal cells, confirming ACE2 as the sole receptor and revealing redundancy in downstream cell surface TMPRSS- and endocytic Cathepsin-mediated pathways. In addition, these data address the implications of SARS-CoV-2 exposure in the setting of the commonly prescribed ACE-inhibitor, lisinopril, confirming its negligible impact on infection of kidney cells. Taken together, these results provide valuable insight into the mechanism of viral infection in the human kidney.
| Authors | Vanslambrouck JM, Neil JA, Rudraraju R, Mah S, Tan KS, Groenewegen E, Forbes TA, Karavendzas K, Elliott DA, Porrello ER, Subbarao K, Little MH |
|---|---|
| Journal | Journal of virology |
| Publication Date | 2024 Mar 19;98(3):e0180223 |
| PubMed | 38334329 |
| PubMed Central | PMC10949421 |
| DOI | 10.1128/jvi.01802-23 |