@article{Paul_T-2022_168270,
title = {Adrenal tropism of SARS-CoV-2 and adrenal findings in a post-mortem case series of patients with severe fatal COVID-19},
author = {Paul, T. and Ledderose, S. and Bartsch, H. and Sun, N. and Soliman, S. and Märkl, B. and Ruf, V. and Herms, J. and Stern, M. and Keppler, O. and Delbridge, C. and Müller, S. and Piontek, G. and Kimoto, Y. and Schreiber, F. and Williams, T. and Neumann, J. and Knösel, T. and Schulz, H. and Spallek, R. and Graw, M. and Kirchner, T. and Walch, A. and Rudelius, M.},
month = {mar},
year = {2022},
abstract = {Progressive respiratory failure and hyperinflammatory response is the primary cause of death in the coronavirus disease 2019 (COVID-19) pandemic. Despite mounting evidence of disruption of the hypothalamus-pituitary-adrenal axis in COVID-19, relatively little is known about the tropism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to adrenal glands and associated changes. Here we demonstrate adrenal viral tropism and replication in COVID-19 patients. Adrenal glands showed inflammation accompanied by inflammatory cell death. Histopathologic analysis revealed widespread microthrombosis and severe adrenal injury. In addition, activation of the glycerophospholipid metabolism and reduction of cortisone intensities were characteristic for COVID-19 specimens. In conclusion, our autopsy series suggests that SARS-CoV-2 facilitates the induction of adrenalitis. Given the central role of adrenal glands in immunoregulation and taking into account the significant adrenal injury observed, monitoring of developing adrenal insufficiency might be essential in acute SARS-CoV-2 infection and during recovery.},
volume = {13},
journal = {Nature Communications},
publisher = {Springer Nature},
url = {https://doi.org/10.1038/s41467-022-29145-3},
}
