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  • SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids #MMPMID35032430
  • Jansen J; Reimer KC; Nagai JS; Varghese FS; Overheul GJ; de Beer M; Roverts R; Daviran D; Fermin LAS; Willemsen B; Beukenboom M; Djudjaj S; von Stillfried S; van Eijk LE; Mastik M; Bulthuis M; Dunnen WD; van Goor H; Hillebrands JL; Triana SH; Alexandrov T; Timm MC; van den Berge BT; van den Broek M; Nlandu Q; Heijnert J; Bindels EMJ; Hoogenboezem RM; Mooren F; Kuppe C; Miesen P; Grunberg K; Ijzermans T; Steenbergen EJ; Czogalla J; Schreuder MF; Sommerdijk N; Akiva A; Boor P; Puelles VG; Floege J; Huber TB; van Rij RP; Costa IG; Schneider RK; Smeets B; Kramann R
  • Cell Stem Cell 2022[Feb]; 29 (2): 217-231.e8 PMID35032430show ga
  • 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.
  • |*COVID-19/complications[MESH]
  • |*SARS-CoV-2[MESH]
  • |Fibrosis[MESH]
  • |Humans[MESH]
  • |Kidney[MESH]
  • |Organoids/pathology[MESH]

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  • suck abstract from ncbi

    217 2.29 2022