Author: Daniel J Butler; Christopher Mozsary; Cem Meydan; David C Danko; Jonathan Foox; Joel Rosiene; Alon Shaiber; Ebrahim Afshinnekoo; Matthew MacKay; Fritz J Sedlazeck; Nikolay A Ivanov; Maria A Sierra; Diana Pohle; Michael Zeitz; Vijendra Ramlall; Undina Gisladottir; Craig D Westover; Krista Ryon; Benjamin Young; Chandrima Bhattacharya; Phyllis Ruggiero; Bradley W Langhorst; Nathan A Tanner; Justyn Gawrys; Dmitry Meleshko; Dong Xu; Jenny Xiang; Angelika Iftner; Daniela Bezdan; John Sipley; Lin Cong; Arryn Craney; Priya Velu; Ari Melnick; Iman A Hajirasouliha; Thomas Iftner; Mirella Salvatore; Massimo Loda; Lars F Westblade; Shawn Levy; Melissa Cushing; Nicholas P Tatonetti; Marcin Imielinski; Hanna Rennert; Christopher Mason
Title: Host, Viral, and Environmental Transcriptome Profiles of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Document date: 2020_4_20
ID: kyoa5gsf_38
Snippet: Although these data alone cannot establish causality between infection and ACE2 expression regulation, they provide some testable hypotheses. For example, if some patients are more susceptible because they are already expressing high levels of ACE2, this could help with targeting ACE2 in these patients as a prophylactic method. However, if the cells respond to infection with ACE2 expression, and this leads to the cytokine storm seen in patients, .....
Document: Although these data alone cannot establish causality between infection and ACE2 expression regulation, they provide some testable hypotheses. For example, if some patients are more susceptible because they are already expressing high levels of ACE2, this could help with targeting ACE2 in these patients as a prophylactic method. However, if the cells respond to infection with ACE2 expression, and this leads to the cytokine storm seen in patients, then this could be used as a downstream treatment (post-infection), for when ACE2 interacts with TMPRSS2, such as the ongoing trials with camostat mesylate (Hoffman et al., 2020) . Moreover, SARS-CoV-2 has been found to induce phosphorylation of STAT1 and increases in ISG proteins, a mechanism not previously seen in SARS-CoV, suggesting a potential molecular mechanism behind the upregulation of interferon response (Lokugamage et al., 2020).
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