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, Andrea A. Barquero, Ana Ceballos, Cybele C. Garcia () and Francisco J. Quintana ()
Additional contact information
Federico Giovannoni: Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Zhaorong Li: Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Federico Remes-Lenicov: Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires
María E. Dávola: Michael DeGroote Institute for Infectious Disease Research, McMaster University
Mercedes Elizalde: Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires
Ana Paletta: Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires
Ali A. Ashkar: Michael DeGroote Institute for Infectious Disease Research, McMaster University
Karen L. Mossman: Michael DeGroote Institute for Infectious Disease Research, McMaster University
Andrea V. Dugour: Instituto de Ciencia y Tecnología Dr. Cesar Milstein (Consejo Nacional de Investigaciones Científicas y Técnicas-Fundacion Cassara)
Juan M. Figueroa: Instituto de Ciencia y Tecnología Dr. Cesar Milstein (Consejo Nacional de Investigaciones Científicas y Técnicas-Fundacion Cassara)
Andrea A. Barquero: Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires. CONICET- Instituto de Química Biológica (IQUIBICEN)
Ana Ceballos: Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires
Cybele C. Garcia: Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires. CONICET- Instituto de Química Biológica (IQUIBICEN)
Francisco J. Quintana: Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School

Nature Communications, 2021, vol. 12, issue 1, 1-12

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-25412-x

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