Evidence map›Paper›PMID 34446714›Full record

ArticleNature communications2021

AHR signaling is induced by infection with coronaviruses.

Federico Giovannoni, Zhaorong Li, Federico Remes-Lenicov, María E Dávola, Mercedes Elizalde, Ana Paletta, Ali A Ashkar, Karen L Mossman, Andrea V Dugour, Juan M Figueroa and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
11.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 81 citations in OpenAlex.

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  19. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 3 countries.

Federico Giovannoni *Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Zhaorong Li *Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-5268-6986
Federico Remes-LenicovInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, Buenos Aires, Argentina.
María E DávolaDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, Michael DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON, Canada.
Mercedes ElizaldeInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, Buenos Aires, Argentina.ORCID 0000-0002-0533-4283
Ana PalettaInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, Buenos Aires, Argentina.
Ali A AshkarDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, Michael DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON, Canada.ORCID 0000-0003-1139-1468
Karen L MossmanDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, Michael DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON, Canada.ORCID 0000-0002-1725-5873
Andrea V DugourInstituto de Ciencia y Tecnología Dr. Cesar Milstein (Consejo Nacional de Investigaciones Científicas y Técnicas-Fundacion Cassara), Buenos Aires, Argentina.
Juan M FigueroaInstituto de Ciencia y Tecnología Dr. Cesar Milstein (Consejo Nacional de Investigaciones Científicas y Técnicas-Fundacion Cassara), Buenos Aires, Argentina.
Andrea A BarqueroLaboratorio de Virología, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires. CONICET- Instituto de Química Biológica (IQUIBICEN), Buenos Aires, Argentina.
Ana CeballosInstituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires, Buenos Aires, Argentina.
Cybele C GarciaLaboratorio de Estrategias Antivirales, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires. CONICET- Instituto de Química Biológica (IQUIBICEN), Buenos Aires, Argentina. cygarcia@qb.fcen.uba.ar.ORCID 0000-0002-6431-7176
Francisco J QuintanaAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. fquintana@rics.bwh.harvard.edu.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad de Buenos Aires · ARMcMaster University · CABrigham and Women's Hospital · USBroad Institute · US

Funding

Multi-omic dissection of the transcriptional, epigenetic, and proteomic signatures of cells infected with latent HIVR01AI149699 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI ABATE, ADAM R., QUINTANA, FRANCISCO J. · 2020 to 2024
$3.8M
AHR-mediated immunosuppression in glioblastomaR01ES029136 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI Francisco J. Quintana, DAVID A REARDON · 2019 to 2026
$3.3M
Regulation of CNS AutoimmunityR01AI126880 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI QUINTANA, FRANCISCO J. · 2017 to 2021
$2.1M
Control of Local CNS InflammationR01NS102807 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI QUINTANA, FRANCISCO J. · 2018 to 2022
$1.8M
Pollution Aggravates Autoimmunity Through the Aryl Hydrocarbon ReceptorR21ES025304 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI MEZRICH, JOSHUA D · 2015 to 2016
$421k
NIAID NIH HHS R01 AI126880NIAID NIH HHS R01 AI149699NIEHS NIH HHS R01 ES029136NIEHS NIH HHS R21 ES025304NINDS NIH HHS R01 NS102807
6 · The paper itself

Abstract

Coronavirus infection in humans is usually associated to respiratory tract illnesses, ranging in severity from mild to life-threatening respiratory failure. The aryl hydrocarbon receptor (AHR) was recently identified as a host factor for Zika and dengue viruses; AHR antagonists boost antiviral immunity, decrease viral titers and ameliorate Zika-induced pathology in vivo. Here we report that AHR is activated by infection with different coronaviruses, potentially impacting antiviral immunity and lung epithelial cells. Indeed, the analysis of single-cell RNA-seq from lung tissue detected increased expression of AHR and AHR transcriptional targets, suggesting AHR signaling activation in SARS-CoV-2-infected epithelial cells from COVID-19 patients. Moreover, we detected an association between AHR expression and viral load in SARS-CoV-2 infected patients. Finally, we found that the pharmacological inhibition of AHR suppressed the replication in vitro of one of the causative agents of the common cold, HCoV-229E, and the causative agent of the COVID-19 pandemic, SARS-CoV-2. Taken together, these findings suggest that AHR activation is a common strategy used by coronaviruses to evade antiviral immunity and promote viral replication, which may also contribute to lung pathology. Future studies should further evaluate the potential of AHR as a target for host-directed antiviral therapy.

Indexed as

Signal TransductionCoronavirusCoronavirus InfectionsCOVID-19Epithelial CellsFemaleHumansMaleReceptors, Aryl HydrocarbonSARS-CoV-2Receptors, Aryl Hydrocarbon

Identifiers

PMID34446714
PMCPMC8390748
OpenAlexW3195151522

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.