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Targeting the catecholamine-cytokine axis to prevent SARS-CoV-2 cytokine storm syndrome
Maximilian F Konig; Mike Powell; Verena Staedtke; Ren-Yuan Bai; David L Thomas; Nicole Fischer; Sakibul Huq; Adham M Khalafallah; Allison Koenecke; Ruoxuan Xiong; Brett Mensh; Nickolas Papadopoulos; Kenneth W Kinzler; Bert Vogelstein; Joshua T Vogelstein; Susan Athey; Shibin Zhou; Chetan Bettegowda.
Afiliación
  • Maximilian F Konig; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA; Division of Rheumat
  • Mike Powell; Department of Biomedical Engineering, Institute of Computational Medicine, The Johns Hopkins University, Baltimore, MD, USA
  • Verena Staedtke; Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Ren-Yuan Bai; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • David L Thomas; Division of Infectious Diseases, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Nicole Fischer; The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Sakibul Huq; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Adham M Khalafallah; Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • Allison Koenecke; Institute for Computational & Mathematical Engineering, Stanford University, Stanford, CA, USA
  • Ruoxuan Xiong; Institute for Computational & Mathematical Engineering, Stanford University, Stanford, CA, USA
  • Brett Mensh; Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA and Optimize Science
  • Nickolas Papadopoulos; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA
  • Kenneth W Kinzler; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA
  • Bert Vogelstein; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA
  • Joshua T Vogelstein; Department of Biomedical Engineering, Institute of Computational Medicine, The Johns Hopkins University, Baltimore, MD, USA
  • Susan Athey; Stanford Graduate School of Business, Stanford University, Stanford, CA, USA
  • Shibin Zhou; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA
  • Chetan Bettegowda; Ludwig Center, Lustgarten Laboratory, and the Howard Hughes Medical Institute at The Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA; Department of Neuro
Preprint en En | PREPRINT-MEDRXIV | ID: ppmedrxiv-20051565
ABSTRACT
In Coronavirus disease 2019 (COVID-19), the initial viral-replication phase is often followed by a hyperinflammatory reaction in the lungs and other organ systems that leads to acute respiratory distress syndrome (ARDS), the need for mechanical ventilation, and death despite maximal supportive care. As no antiviral treatments have yet proven effective, efforts to prevent progression to the severe stages of COVID-19 without inhibiting antiviral immune responses are desperately needed. We have previously demonstrated that a common, inexpensive, and well-tolerated class of drugs called alpha-1 adrenergic receptor (1-AR) antagonists can prevent hyperinflammation ("cytokine storm") and death in mice. We here present clinical data that supports the use of 1-AR antagonists in the prevention of severe complications of pneumonia, ARDS, and COVID-19.
Licencia
cc_by_nc_nd
Texto completo: 1 Colección: 09-preprints Base de datos: PREPRINT-MEDRXIV Tipo de estudio: Prognostic_studies Idioma: En Año: 2020 Tipo del documento: Preprint
Texto completo: 1 Colección: 09-preprints Base de datos: PREPRINT-MEDRXIV Tipo de estudio: Prognostic_studies Idioma: En Año: 2020 Tipo del documento: Preprint