The AI-discovered aetiology of COVID-19 and rationale of the irinotecan+ etoposide combination therapy for critically ill COVID-19 patients
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Abstract
We present the AI-discovered aetiology of COVID-19, based on a precise disease model of COVID-19 built under
five weeks that best matches the epidemiological characteristics, transmission dynamics, clinical features, and
biological properties of COVID-19 and consistently explains the rapidly expanding COVID-19 literature. We
present that SARS-CoV-2 implements a unique unbiased survival strategy of balancing viral replication with viral
spread by increasing its dependence on (i) ACE2-expressing cells for viral entry and spread, (ii) PI3K signaling in
ACE2-expressing cells for viral replication and egress, and (iii) viral- non-structural-and-accessory-protein-dependent immunomodulation to balance viral spread and viral replication. We further propose the combination of
irinotecan (an in-market topoisomerase I inhibitor) and etoposide (an in-market topoisomerase II inhibitor)
could potentially be an exceptionally effective treatment to protect critically ill patients from death caused by
COVID-19-specific cytokine storms triggered by sepsis, ARDS, and other fatal comorbidities.
Palabras clave
Aetiology; Treatment; Cytokine storm; ICU; COVID-19; ACE2; Irinotecan; Etoposide; SARS-CoV-2Link to resource
https://doi.org/10.1016/j.mehy.2020.110180Collections
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