<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Daniloski, Zharko</style></author><author><style face="normal" font="default" size="100%">Jordan, Tristan X</style></author><author><style face="normal" font="default" size="100%">Wessels, Hans-Hermann</style></author><author><style face="normal" font="default" size="100%">Hoagland, Daisy A</style></author><author><style face="normal" font="default" size="100%">Kasela, Silva</style></author><author><style face="normal" font="default" size="100%">Legut, Mateusz</style></author><author><style face="normal" font="default" size="100%">Maniatis, Silas</style></author><author><style face="normal" font="default" size="100%">Mimitou, Eleni P</style></author><author><style face="normal" font="default" size="100%">Lu, Lu</style></author><author><style face="normal" font="default" size="100%">Geller, Evan</style></author><author><style face="normal" font="default" size="100%">Danziger, Oded</style></author><author><style face="normal" font="default" size="100%">Rosenberg, Brad R</style></author><author><style face="normal" font="default" size="100%">Phatnani, Hemali</style></author><author><style face="normal" font="default" size="100%">Smibert, Peter</style></author><author><style face="normal" font="default" size="100%">Lappalainen, Tuuli</style></author><author><style face="normal" font="default" size="100%">tenOever, Benjamin R</style></author><author><style face="normal" font="default" size="100%">Sanjana, Neville E</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Identification of Required Host Factors for SARS-CoV-2 Infection in Human Cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">A549 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Alveolar Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Angiotensin-Converting Enzyme 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Biosynthetic Pathways</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol</style></keyword><keyword><style  face="normal" font="default" size="100%">Clustered Regularly Interspaced Short Palindromic Repeats</style></keyword><keyword><style  face="normal" font="default" size="100%">COVID-19</style></keyword><keyword><style  face="normal" font="default" size="100%">Endosomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockout Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">rab GTP-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">rab7 GTP-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Interference</style></keyword><keyword><style  face="normal" font="default" size="100%">SARS-CoV-2</style></keyword><keyword><style  face="normal" font="default" size="100%">Single-Cell Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Load</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2021</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2021 01 07</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">184</style></volume><pages><style face="normal" font="default" size="100%">92-105.e16</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;To better understand host-virus genetic dependencies and find potential therapeutic targets for COVID-19, we performed a genome-scale CRISPR loss-of-function screen to identify host factors required for SARS-CoV-2 viral infection of human alveolar epithelial cells. Top-ranked genes cluster into distinct pathways, including the vacuolar ATPase proton pump, Retromer, and Commander complexes. We validate these gene targets using several orthogonal methods such as CRISPR knockout, RNA interference knockdown, and small-molecule inhibitors. Using single-cell RNA-sequencing, we identify shared transcriptional changes in cholesterol biosynthesis upon loss of top-ranked genes. In addition, given the key role of the ACE2 receptor in the early stages of viral entry, we show that loss of RAB7A reduces viral entry by sequestering the ACE2 receptor inside cells. Overall, this work provides a genome-scale, quantitative resource of the impact of the loss of each host gene on fitness/response to viral infection.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/33147445?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sajuthi, Satria P</style></author><author><style face="normal" font="default" size="100%">DeFord, Peter</style></author><author><style face="normal" font="default" size="100%">Li, Yingchun</style></author><author><style face="normal" font="default" size="100%">Jackson, Nathan D</style></author><author><style face="normal" font="default" size="100%">Montgomery, Michael T</style></author><author><style face="normal" font="default" size="100%">Everman, Jamie L</style></author><author><style face="normal" font="default" size="100%">Rios, Cydney L</style></author><author><style face="normal" font="default" size="100%">Pruesse, Elmar</style></author><author><style face="normal" font="default" size="100%">Nolin, James D</style></author><author><style face="normal" font="default" size="100%">Plender, Elizabeth G</style></author><author><style face="normal" font="default" size="100%">Wechsler, Michael E</style></author><author><style face="normal" font="default" size="100%">Mak, Angel C Y</style></author><author><style face="normal" font="default" size="100%">Eng, Celeste</style></author><author><style face="normal" font="default" size="100%">Salazar, Sandra</style></author><author><style face="normal" font="default" size="100%">Medina, Vivian</style></author><author><style face="normal" font="default" size="100%">Wohlford, Eric M</style></author><author><style face="normal" font="default" size="100%">Huntsman, Scott</style></author><author><style face="normal" font="default" size="100%">Nickerson, Deborah A</style></author><author><style face="normal" font="default" size="100%">Germer, Soren</style></author><author><style face="normal" font="default" size="100%">Zody, Michael C</style></author><author><style face="normal" font="default" size="100%">Abecasis, Gonçalo</style></author><author><style face="normal" font="default" size="100%">Kang, Hyun Min</style></author><author><style face="normal" font="default" size="100%">Rice, Kenneth M</style></author><author><style face="normal" font="default" size="100%">Kumar, Rajesh</style></author><author><style face="normal" font="default" size="100%">Oh, Sam</style></author><author><style face="normal" font="default" size="100%">Rodriguez-Santana, Jose</style></author><author><style face="normal" font="default" size="100%">Burchard, Esteban G</style></author><author><style face="normal" font="default" size="100%">Seibold, Max A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Commun</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat Commun</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Angiotensin-Converting Enzyme 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Betacoronavirus</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Coronavirus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">COVID-19</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Variation</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Interferons</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-13</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Nasal Mucosa</style></keyword><keyword><style  face="normal" font="default" size="100%">Pandemics</style></keyword><keyword><style  face="normal" font="default" size="100%">Peptidyl-Dipeptidase A</style></keyword><keyword><style  face="normal" font="default" size="100%">Pneumonia, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">SARS-CoV-2</style></keyword><keyword><style  face="normal" font="default" size="100%">Serine Endopeptidases</style></keyword><keyword><style  face="normal" font="default" size="100%">Virus Internalization</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2020 10 12</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">11</style></volume><pages><style face="normal" font="default" size="100%">5139</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2, an emerging virus that utilizes host proteins ACE2 and TMPRSS2 as entry factors. Understanding the factors affecting the pattern and levels of expression of these genes is important for deeper understanding of SARS-CoV-2 tropism and pathogenesis. Here we explore the role of genetics and co-expression networks in regulating these genes in the airway, through the analysis of nasal airway transcriptome data from 695 children. We identify expression quantitative trait loci for both ACE2 and TMPRSS2, that vary in frequency across world populations. We find TMPRSS2 is part of a mucus secretory network, highly upregulated by type 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to respiratory viruses highly upregulates ACE2 expression. IL-13 and virus infection mediated effects on ACE2 expression were also observed at the protein level in the airway epithelium. Finally, we define airway responses to common coronavirus infections in children, finding that these infections generate host responses similar to other viral species, including upregulation of IL6 and ACE2. Our results reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/33046696?dopt=Abstract</style></custom1></record></records></xml>