TY - JOUR
T1 - Leveraging publicly available coronavirus data to identify new therapeutic targets for COVID-19
AU - Sell, Stacy L.
AU - Prough, Donald S.
AU - Weisz, Harris A.
AU - Widen, Steve G.
AU - Hellmich, Helen L.
N1 - Publisher Copyright:
© 2021 Sell et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2021/9
Y1 - 2021/9
N2 - Many important questions remain regarding severe acute respiratory syndrome coronavirus- 2 (SARS-CoV-2), the viral pathogen responsible for COVID-19. These questions include the mechanisms explaining the high percentage of asymptomatic but highly infectious individuals, the wide variability in disease susceptibility, and the mechanisms of longlasting debilitating effects. Bioinformatic analysis of four coronavirus datasets representing previous outbreaks (SARS-CoV-1 and MERS-CoV), as well as SARS-CoV-2, revealed evidence of diverse host factors that appear to be coopted to facilitate virus-induced suppression of interferon-induced innate immunity, promotion of viral replication and subversion and/or evasion of antiviral immune surveillance. These host factors merit further study given their postulated roles in COVID-19-induced loss of smell and brain, heart, vascular, lung, liver, and gut dysfunction.
AB - Many important questions remain regarding severe acute respiratory syndrome coronavirus- 2 (SARS-CoV-2), the viral pathogen responsible for COVID-19. These questions include the mechanisms explaining the high percentage of asymptomatic but highly infectious individuals, the wide variability in disease susceptibility, and the mechanisms of longlasting debilitating effects. Bioinformatic analysis of four coronavirus datasets representing previous outbreaks (SARS-CoV-1 and MERS-CoV), as well as SARS-CoV-2, revealed evidence of diverse host factors that appear to be coopted to facilitate virus-induced suppression of interferon-induced innate immunity, promotion of viral replication and subversion and/or evasion of antiviral immune surveillance. These host factors merit further study given their postulated roles in COVID-19-induced loss of smell and brain, heart, vascular, lung, liver, and gut dysfunction.
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U2 - 10.1371/journal.pone.0257965
DO - 10.1371/journal.pone.0257965
M3 - Article
C2 - 34587192
AN - SCOPUS:85116035918
SN - 1932-6203
VL - 16
JO - PloS one
JF - PloS one
IS - 9 September
M1 - e0257965
ER -