@article {1024,
	title = {SARS-CoV-2 induces human plasmacytoid predendritic cell diversification via UNC93B and IRAK4.},
	journal = {J Exp Med},
	volume = {218},
	year = {2021},
	month = {2021 04 05},
	abstract = {<p>Several studies have analyzed antiviral immune pathways in late-stage severe COVID-19. However, the initial steps of SARS-CoV-2 antiviral immunity are poorly understood. Here we have isolated primary SARS-CoV-2 viral strains and studied their interaction with human plasmacytoid predendritic cells (pDCs), a key player in antiviral immunity. We show that pDCs are not productively infected by SARS-CoV-2. However, they efficiently diversified into activated P1-, P2-, and P3-pDC effector subsets in response to viral stimulation. They expressed CD80, CD86, CCR7, and OX40 ligand at levels similar to influenza virus-induced activation. They rapidly produced high levels of interferon-α, interferon-λ1, IL-6, IP-10, and IL-8. All major aspects of SARS-CoV-2-induced pDC activation were inhibited by hydroxychloroquine. Mechanistically, SARS-CoV-2-induced pDC activation critically depended on IRAK4 and UNC93B1, as established using pDC from genetically deficient patients. Overall, our data indicate that human pDC are efficiently activated by SARS-CoV-2 particles and may thus contribute to type I IFN-dependent immunity against SARS-CoV-2 infection.</p>},
	keywords = {Biomarkers, Cell Plasticity, COVID-19, Cytokines, Dendritic Cells, Host-Pathogen Interactions, Humans, Hydroxychloroquine, Immunomodulation, Immunophenotyping, Inflammation Mediators, Interferon Type I, Interferons, Interleukin-1 Receptor-Associated Kinases, Membrane Transport Proteins, SARS-CoV-2},
	issn = {1540-9538},
	doi = {10.1084/jem.20201387},
	author = {Onodi, Fanny and Bonnet-Madin, Lucie and Meertens, Laurent and Karpf, L{\'e}a and Poirot, Justine and Zhang, Shen-Ying and Picard, Capucine and Puel, Anne and Jouanguy, Emmanuelle and Zhang, Qian and Le Goff, J{\'e}r{\^o}me and Molina, Jean-Michel and Delaugerre, Constance and Casanova, Jean-Laurent and Amara, Ali and Soumelis, Vassili}
}
@article {844,
	title = {Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium.},
	journal = {Nat Commun},
	volume = {11},
	year = {2020},
	month = {2020 10 12},
	pages = {5139},
	abstract = {<p>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.</p>},
	keywords = {Angiotensin-Converting Enzyme 2, Betacoronavirus, Child, Coronavirus Infections, COVID-19, Epithelial Cells, Gene Expression Profiling, Gene Expression Regulation, Genetic Variation, Host-Pathogen Interactions, Humans, Inflammation, Interferons, Interleukin-13, Middle Aged, Nasal Mucosa, Pandemics, Peptidyl-Dipeptidase A, Pneumonia, Viral, SARS-CoV-2, Serine Endopeptidases, Virus Internalization},
	issn = {2041-1723},
	doi = {10.1038/s41467-020-18781-2},
	author = {Sajuthi, Satria P and DeFord, Peter and Li, Yingchun and Jackson, Nathan D and Montgomery, Michael T and Everman, Jamie L and Rios, Cydney L and Pruesse, Elmar and Nolin, James D and Plender, Elizabeth G and Wechsler, Michael E and Mak, Angel C Y and Eng, Celeste and Salazar, Sandra and Medina, Vivian and Wohlford, Eric M and Huntsman, Scott and Nickerson, Deborah A and Germer, Soren and Zody, Michael C and Abecasis, Gon{\c c}alo and Kang, Hyun Min and Rice, Kenneth M and Kumar, Rajesh and Oh, Sam and Rodriguez-Santana, Jose and Burchard, Esteban G and Seibold, Max A}
}
