@article{Jansen_J-2022_130957,
title = {SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids},
author = {Jansen, J. and Reimer, K. and Nagai, J. and Varghese, F. and Overheul, G. and de Beer, M. and Roverts, R. and Daviran, D. and Fermin, L. and Willemsen, B. and Beukenboom, M. and Djudjaj, S. and von Stillfried, S. and van Eijk, L. and Mastik, M. and Bulthuis, M. and den Dunnen, W. and van Goor, H. and Hillebrands, J. and Triana, S. and Alexandrov, T. and Timm, M. and van den Berge, B. and van den Broek, M. and Nlandu, Q. and Heijnert, J. and Bindels, E. and Hoogenboezem, R. and Mooren, F. and Kuppe, C. and Kramann, R.},
month = {feb},
year = {2022},
abstract = {Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human-induced pluripotent stem cell-derived kidney organoids with SARS-CoV-2. Single-cell RNA sequencing indicated injury and dedifferentiation of infected cells with activation of profibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in long COVID.},
pages = {217-231},
volume = {29},
issue = {2},
journal = {Cell Stem Cell},
publisher = {Elsevier},
url = {https://doi.org/10.1016/j.stem.2021.12.010},
}
