About: In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age

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About: In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age
Creator	Jerome, Keith Shi, Pei-Yong Moscona, Anne Porotto, Matteo Cajimat, Maria Huang, Meei-Li Bente, Dennis Shrestha, Lasata Xie, Hong Bovier, Francesca Greninger, Peddu, Vikas Lieberman, Nicole Mears, Pavitra,
Source	BioRxiv; Medline
abstract	Despite limited genomic diversity, SARS-CoV-2 has shown a wide range of clinical manifestations in different patient populations. The mechanisms behind these host differences are still unclear. Here, we examined host response gene expression across infection status, viral load, age, and sex among shotgun RNA-sequencing profiles of nasopharyngeal swabs from 430 individuals with PCR-confirmed SARS-CoV-2 and 54 negative controls. SARS-CoV-2 induced a strong antiviral response with upregulation of antiviral factors such as OAS1-3 and IFIT1-3, and Th1 chemokines CXCL9/10/11, as well as a reduction in transcription of ribosomal proteins. SARS-CoV-2 culture in human airway epithelial cultures replicated the in vivo antiviral host response. Patient-matched longitudinal specimens (mean elapsed time = 6.3 days) demonstrated reduction in interferon-induced transcription, recovery of transcription of ribosomal proteins, and initiation of wound healing and humoral immune responses. Expression of interferon-responsive genes, including ACE2, increased as a function of viral load, while transcripts for B cell-specific proteins and neutrophil chemokines were elevated in patients with lower viral load. Older individuals had reduced expression of Th1 chemokines CXCL9/10/11 and their cognate receptor, CXCR3, as well as CD8A and granzyme B, suggesting deficiencies in trafficking and/or function of cytotoxic T cells and natural killer (NK) cells. Relative to females, males had reduced B and NK cell-specific transcripts and an increase in inhibitors of NF-κB signaling, possibly inappropriately throttling antiviral responses. Collectively, our data demonstrate that host responses to SARS-CoV-2 are dependent on viral load and infection time course, with observed differences due to age and sex that may contribute to disease severity.
has issue date	2020-06-22(xsd:dateTime)
bibo:doi	10.1101/2020.06.22.165225
bibo:pmid	32607510
has license	biorxiv
sha1sum (hex)	d5fa1ff4d98c18a644d4ebdc49b61a5f1bec6024
schema:url	https://doi.org/10.1101/2020.06.22.165225
resource representing a document's title	In vivo antiviral host response to SARS-CoV-2 by viral load, sex, and age
has PubMed identifier	32607510
schema:publication	bioRxiv
resource representing a document's body	covid:d5fa1ff4d98c18a644d4ebdc49b61a5f1bec6024#body_text
is schema:about of	named entity 'transcripts' named entity 'Despite' named entity 'trafficking' named entity 'upregulation' named entity 'throttling' named entity 'signaling' named entity 'SARS-CoV-2' named entity 'host response' named entity 'PATIENT' named entity 'UNCLEAR' named entity 'EXPRESSION' named entity 'RESPONSES' named entity 'POSSIBLY' named entity 'NASOPHARYNGEAL' named entity 'CHEMOKINES' named entity 'DEMONSTRATED' named entity 'host response' named entity 'response' named entity 'neutrophil' named entity 'reduced' named entity 'gene' named entity 'granzyme' named entity 'individuals' named entity 'ribosomal proteins' named entity 'wound healing' named entity 'negative' named entity 'males' named entity 'reduction' named entity 'SARS-CoV-2' named entity 'CXCL9' named entity 'ribosomal proteins' named entity 'Short' named entity 'NK cell' named entity 'Th1' named entity 'CD8A' named entity 'nasopharyngeal swabs' named entity 'neutrophil' named entity 'SARS-CoV-2' named entity 'interferon' named entity 'epithelial' named entity 'PCR' named entity 'chemokines' named entity 'viral load' named entity 'antiviral' named entity 'ribosomal proteins' named entity 'SARS-CoV-2' named entity 'host response' named entity 'Short Title' named entity 'data' named entity 'infection' named entity 'coinfections' named entity 'natural killer' named entity 'CXCL9' named entity 'downregulated' named entity 'SARS-CoV-2' named entity 'NK cell' named entity 'bacteria' named entity 'receptor' named entity 'infection' named entity 'TFPI' named entity 'CD8A' named entity 'dendritic cell' named entity 'repressor' named entity 'SARS-CoV-2' named entity 'GZMB' named entity 'viral load' named entity 'SARS-CoV-2' named entity 'effector T cell'

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