Lovetrue, Bragi
2020-09-22T20:49:21Z
2020-09-22T20:49:21Z
2020
0306-9877
https://doi.org/10.1016/j.mehy.2020.110180
http://hdl.handle.net/20.500.12010/13618
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.
4 páginas
application/pdf
eng
Medical Hypotheses
reponame:Expeditio Repositorio Institucional UJTL
instname:Universidad de Bogotá Jorge Tadeo Lozano
Aetiology
Treatment
Cytokine storm
ICU
COVID-19
ACE2
Irinotecan
Etoposide
SARS-CoV-2
The AI-discovered aetiology of COVID-19 and rationale of the irinotecan+ etoposide combination therapy for critically ill COVID-19 patients
Artículo
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/acceptedVersion
Abierto (Texto Completo)
https://doi.org/10.1016/j.mehy.2020.110180
http://purl.org/coar/resource_type/c_2df8fbb1