Selected article for: "host receptor and previous study"
Author: Satria P. Sajuthi; Peter DeFord; Nathan D. Jackson; Michael T. Montgomery; Jamie L. Everman; Cydney L. Rios; Elmar Pruesse; James D. Nolin; Elizabeth G. Plender; Michael E. Wechsler; Angel CY Mak; Celeste Eng; Sandra Salazar; Vivian Medina; Eric M. Wohlford; Scott Huntsman; Deborah A. Nickerson; Soren Germer; Michael C. Zody; Gonçalo Abecasis; Hyun Min Kang; Kenneth M. Rice; Rajesh Kumar; Sam Oh; Jose Rodriguez-Santana; Esteban G. Burchard; Max A. Seibold
Title: Type 2 and interferon inflammation strongly regulate SARS-CoV-2 related gene expression in the airway epithelium
  • Document date: 2020_4_10
    • ID: mj8ebo7i_13
    Snippet: This information is interesting in several regards. First, it suggests that SARS-CoV-2 472 and other coronaviruses using ACE2 as a receptor could leverage the host anti-viral 473 response to increase the infectability of airway cells. Secondly, as data here and 474 elsewhere show, asymptomatic carriage of respiratory viruses is common, especially in 475 young children 19, 28-31 . Children in the GALA II cohort included in this study ranged in 476.....
    Document: This information is interesting in several regards. First, it suggests that SARS-CoV-2 472 and other coronaviruses using ACE2 as a receptor could leverage the host anti-viral 473 response to increase the infectability of airway cells. Secondly, as data here and 474 elsewhere show, asymptomatic carriage of respiratory viruses is common, especially in 475 young children 19, 28-31 . Children in the GALA II cohort included in this study ranged in 476 age from 8-21 years; among them we found 18% who were carrying respiratory viruses 477 without illness. However, as we show in this and our previous study 19 The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.04.09.034454 doi: bioRxiv preprint Our evaluation of genetic influences on airway ACE2 and TMPRSS2 expression 491 revealed a single rare eQTL for ACE2 and several more frequent eQTL variants for 492 TMPRSS2. While both the effect size and explanatory power of these variants paled in 493 comparison to the influence of T2 inflammation and interferon signaling in multi-variable 494 modeling of expression for these genes, the effect of these variants may still be strong 495 enough to alter infection rates and or illness severity, especially in the populations 496

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